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Vasomotor

Vasomotor refers to the neural and muscular mechanisms that regulate the caliber of blood vessels by controlling their constriction (vasoconstriction) and dilation (vasodilation), primarily through the autonomic nervous system.^[1]^[2] This process is essential for maintaining blood pressure, directing blood flow to tissues, and responding to environmental changes such as temperature or stress.^[3] The vasomotor center, located in the medulla oblongata of the brainstem, serves as the primary integration site for these controls, receiving inputs from baroreceptors, chemoreceptors, and higher brain regions to adjust vascular tone via sympathetic efferent nerves.^[4] Sympathetic stimulation releases norepinephrine, which binds to alpha-adrenergic receptors on vascular smooth muscle to induce constriction,^[5] while factors like nitric oxide from the endothelium promote relaxation and dilation.^[6] Vasomotor tone represents the baseline partial constriction of blood vessels due to ongoing sympathetic activity, which is dynamically modulated to ensure adequate perfusion and prevent conditions like hypotension or hypertension.^[7]^[6] Dysregulation of vasomotor function is implicated in cardiovascular disorders, including essential hypertension and Raynaud's phenomenon.^[3] In clinical contexts, the term also describes symptoms arising from vasomotor instability, such as hot flashes during menopause or rhinitis triggered by non-allergic factors,^[8] though these stem from the same underlying vascular control principles.^[9]

Definition and Basics

Definition

Vasomotor refers to the physiological processes involving the constriction (vasoconstriction) or dilation (vasodilation) of blood vessels, which modulate their diameter and thereby regulate blood flow and distribution throughout the body.^[10] These dynamic adjustments primarily occur in arteries and arterioles, enabling precise control over peripheral resistance and perfusion to tissues.^[6] The core mechanism of vasomotor activity centers on the contraction and relaxation of vascular smooth muscle cells located in the tunica media, the middle layer of the vessel wall. These cells respond to various stimuli, generating force that narrows or widens the lumen to influence hemodynamic parameters.^[11] Unlike veins, where compliance dominates, the tunica media in arteries and arterioles provides the structural basis for active tone maintenance through these smooth muscle interactions.^[12] The term "vasomotor" emerged in the mid-19th century to describe neural and other influences on vessel caliber, building on discoveries of vasomotor nerves by Claude Bernard in 1851, who demonstrated sympathetic control over cutaneous vasodilation.^[13] Early foundational studies, such as those by Bayliss and Starling in 1894, explored vasomotor influences on venous and capillary pressures, highlighting how active neural and local factors alter vascular tone independent of passive mechanical distension. This distinction underscores that vasomotor effects represent regulated, physiological responses rather than mere elastic deformation from intravascular pressure changes.^[14]

Vasoconstriction and Vasodilation

Vasoconstriction refers to the narrowing of blood vessel lumens through the contraction of vascular smooth muscle cells, which elevates peripheral vascular resistance and diminishes blood flow to specific tissues.^[11] This process is primarily initiated by an elevation in intracellular calcium ion (Ca²⁺) concentration within the smooth muscle cells.^[15] The increased Ca²⁺ binds to calmodulin, forming a calcium-calmodulin complex that activates myosin light chain kinase (MLCK).^[11] This activation leads to phosphorylation of the myosin light chain, facilitating cross-bridge cycling between actin and myosin filaments and culminating in muscle contraction.^[15] Sympathetic nerves can trigger this vasoconstrictive response through activation of these cellular pathways.^[16] In contrast, vasodilation involves the widening of blood vessel lumens due to relaxation of vascular smooth muscle cells, which lowers resistance and enhances blood flow.^[7] A central mechanism for vasodilation is the hyperpolarization of the smooth muscle cell membrane, often mediated by the opening of potassium channels such as large-conductance calcium-activated potassium (BKCa) channels.^[7] This hyperpolarization reduces the opening probability of voltage-gated calcium channels, thereby limiting Ca²⁺ influx and lowering intracellular Ca²⁺ levels, which promotes dephosphorylation of myosin light chain and muscle relaxation.^[17] The profound effects of vasoconstriction and vasodilation on hemodynamics are quantified by Poiseuille's law, which describes the relationship between vessel radius and resistance.^[18] According to this principle, vascular resistance R is expressed as

R = \frac{8 \eta L}{\pi r^4},

where \eta is the viscosity of blood, L is the length of the vessel, and r is the radius.^[18] The inverse fourth-power dependence on radius means that modest changes in vessel diameter—such as a 10% reduction—can increase resistance by approximately 52%, dramatically altering blood flow.^[18] An important intrinsic contributor to vasoconstriction is the myogenic response, an autoregulatory property of vascular smooth muscle cells that causes contraction in direct response to increased transmural pressure or mechanical stretch.^[19] This response involves stretch-activated ion channels that depolarize the cell membrane, leading to Ca²⁺ entry and activation of the contractile machinery, thereby stabilizing blood flow against pressure fluctuations.^[20]

Control Mechanisms

Neural Control

The vasomotor center, located in the rostral ventrolateral medulla (RVLM), serves as the primary integrative site for central regulation of vasomotor activity, receiving inputs from baroreceptors, chemoreceptors, and higher brain regions to adjust sympathetic outflow to the vasculature.^[21] This center coordinates tonic and phasic sympathetic activity, ensuring appropriate vascular tone in response to physiological demands.^[22] Baroreceptor afferents from the carotid sinus and aortic arch provide inhibitory signals during pressure elevations, while chemoreceptor inputs from the carotid body and higher centers, such as the hypothalamus, facilitate excitatory drive.^[23] Sympathetic innervation predominates in the control of vasomotor function, with postganglionic sympathetic fibers innervating vascular smooth muscle cells throughout most arterial and venous beds. These fibers release norepinephrine, which binds to α1-adrenergic receptors on the smooth muscle, triggering G-protein-coupled activation of phospholipase C, increased intracellular calcium, and subsequent vasoconstriction.^[24] Additionally, adenosine triphosphate (ATP) acts as a co-transmitter from the same vesicles, contributing to the rapid initial phase of vasoconstriction through purinergic P2X receptors before norepinephrine's slower, sustained effects.^[25] Parasympathetic influence on vasomotor activity is limited and indirect in most vascular beds, lacking widespread direct innervation to blood vessels. However, in select regions such as the salivary glands, parasympathetic postganglionic fibers release acetylcholine that activates muscarinic receptors on endothelial cells, promoting localized vasodilation to support glandular secretion.^[26] This contrasts with the dominant sympathetic vasoconstrictor tone elsewhere.^[27] Key reflex arcs modulate vasomotor responses via neural pathways. The baroreflex arc, activated by hypertension, inhibits RVLM activity through vagal and glossopharyngeal afferents, reducing sympathetic outflow and facilitating vasodilation to normalize pressure.^[28] Conversely, the chemoreflex, triggered by hypoxia, excites the RVLM via carotid body afferents, enhancing sympathetic discharge and inducing vasoconstriction in non-essential beds to redirect blood flow.^[29] These reflexes provide rapid, localized adjustments to vasomotor tone.

Endothelial and Local Factors

Endothelial cells serve as a critical barrier and signal transducer in the vascular wall, regulating vasomotor tone through the release of paracrine factors. These cells produce nitric oxide (NO) via endothelial nitric oxide synthase (eNOS), which is activated by stimuli such as shear stress or agonists like acetylcholine. The generated NO diffuses to adjacent vascular smooth muscle cells, where it activates soluble guanylate cyclase, catalyzing the conversion of GTP to cyclic GMP (cGMP). Elevated cGMP levels then activate protein kinase G, leading to dephosphorylation of myosin light chains and reduced intracellular calcium, ultimately causing smooth muscle relaxation and vasodilation.^[30] In contrast, endothelial cells also synthesize potent vasoconstrictors, notably endothelin-1 (ET-1), a 21-amino acid peptide derived from the precursor big ET-1 through cleavage by endothelin-converting enzyme. ET-1 acts primarily on ETA receptors located on vascular smooth muscle cells, triggering G-protein-coupled signaling that increases intracellular calcium via phospholipase C and inositol trisphosphate pathways, resulting in smooth muscle contraction and vasoconstriction. This mechanism maintains baseline vascular tone and responds to local stimuli like hypoxia.^[31] Local metabolic factors from surrounding tissues further modulate vasomotor responses, particularly during increased metabolic demand. Adenosine, released from degrading ATP in hypoxic or ischemic conditions, binds to A2 receptors on smooth muscle and endothelium, activating adenylate cyclase to raise cAMP levels and promote hyperpolarization through potassium channel opening, thereby inducing vasodilation. Similarly, elevated extracellular potassium (K+) from active tissues activates inward-rectifier potassium channels and the Na+/K+-ATPase pump, causing membrane hyperpolarization and relaxation of vascular smooth muscle. Acidosis, marked by increased hydrogen ions (H+), contributes to vasodilation by sensitizing potassium channels and shifting the oxygen-hemoglobin dissociation curve to enhance oxygen delivery.^[32] Shear stress induced by blood flow provides an additional local cue for vasomotor control, stimulating eNOS activation in endothelial cells to release NO and facilitate flow-mediated dilation. This endothelium-dependent process ensures that vessels adapt to changes in flow velocity, maintaining efficient perfusion without external neural input.^[32] Vascular autoregulation integrates these intrinsic mechanisms to sustain constant blood flow across varying perfusion pressures, approximately 60-160 mmHg in many organs, such as the brain.^[33] The myogenic response involves direct stretch-sensitive depolarization of smooth muscle in response to increased transmural pressure, leading to calcium influx and constriction to counteract excessive flow. Metabolic responses complement this by amplifying vasodilation when tissue oxygen or nutrient delivery falls, as detected by local factors like adenosine and H+. Together, these ensure organ-specific stability, such as in the brain and kidneys, independent of systemic influences.^[34]

Humoral Factors

Humoral factors encompass circulating hormones and peptides secreted by endocrine glands that exert systemic effects on vasomotor tone, influencing vascular smooth muscle contraction or relaxation through specific receptor-mediated pathways. These factors typically act with slower onset and longer duration compared to neural mechanisms, contributing to the maintenance of vascular homeostasis under varying physiological conditions. Catecholamines, primarily epinephrine and norepinephrine released from the adrenal medulla, play a key role in modulating vasomotor activity. Epinephrine binds to β2-adrenergic receptors on vascular smooth muscle in skeletal muscle beds, promoting vasodilation via Gs-coupled activation that increases cyclic AMP and relaxes smooth muscle.^[35] In contrast, both epinephrine and norepinephrine activate α1-adrenergic receptors on vascular smooth muscle in most other tissues, inducing vasoconstriction through Gq-coupled signaling that elevates intracellular calcium.^[35] Norepinephrine exhibits higher affinity for these α1 receptors, making it a potent systemic vasoconstrictor.^[35] The renin-angiotensin-aldosterone system (RAAS) provides another major humoral pathway for vasoconstriction. Angiotensin II, generated from angiotensin I by angiotensin-converting enzyme, binds to AT1 receptors on vascular smooth muscle, triggering Gq-protein activation, phospholipase C stimulation, and increased intracellular Ca²⁺, which directly causes vasoconstriction in arterioles.^[36] Aldosterone, stimulated by angiotensin II, indirectly enhances vascular tone by promoting sodium retention and water reabsorption in the kidneys, leading to increased blood volume and sustained elevation of systemic pressure.^[36] Vasopressin, also known as antidiuretic hormone (ADH), acts as a potent vasoconstrictor, particularly in response to conditions like hemorrhage. It binds to V1a receptors on vascular smooth muscle, activating phospholipase C and mobilizing intracellular Ca²⁺ through two concentration-dependent pathways: a low-concentration PKC- and voltage-sensitive Ca²⁺ channel-dependent mechanism, and a high-concentration pathway involving initial Ca²⁺ release from sarcoplasmic reticulum stores.^[37] This response helps maintain blood pressure by shunting blood to vital organs during hypovolemia.^[37] Among humoral dilators, atrial natriuretic peptide (ANP), secreted by atrial myocytes in response to volume expansion, promotes vasodilation by binding to natriuretic peptide receptor-A (NPR-A), a particulate guanylyl cyclase that elevates cyclic GMP (cGMP) levels in vascular smooth muscle, leading to relaxation and reduced systemic vascular resistance.^[38] Similarly, bradykinin induces vasodilation primarily through B2 receptor activation, which stimulates nitric oxide release from endothelium, subsequently increasing cGMP in smooth muscle via soluble guanylyl cyclase, although circulating levels contribute to systemic effects.^[39]

Physiological Functions

Blood Pressure Regulation

Vasomotor tone, maintained by the continuous partial contraction of vascular smooth muscle in arterioles, establishes the basal level of peripheral resistance (PR), which is a primary determinant of mean arterial pressure (MAP). The relationship is expressed as MAP = cardiac output (CO) × PR, where adjustments in arteriolar tone allow for fine-tuning of PR to stabilize blood pressure under varying physiological demands.^[40]^[41] Baroreceptor feedback plays a central role in vasomotor regulation of blood pressure, with carotid sinus and aortic arch baroreceptors detecting acute changes in arterial pressure and relaying signals to the vasomotor center in the medulla oblongata. This negative feedback loop modulates sympathetic outflow to arterioles: increased pressure enhances baroreceptor firing, inhibiting the vasomotor center and promoting vasodilation to reduce PR and MAP, while decreased pressure has the opposite effect, eliciting vasoconstriction to restore homeostasis.^[42]^[43] In short-term blood pressure control, sympathetic-mediated vasoconstriction is crucial during orthostatic stress, such as standing, where gravitational pooling in the lower body reduces venous return and CO, prompting rapid arteriolar constriction to elevate PR and prevent hypotension. Similarly, during exercise, heightened sympathetic activity induces vasoconstriction in non-active vascular beds to redistribute blood flow to working muscles while maintaining overall MAP against increased metabolic demands.^[44]^[45] Long-term blood pressure regulation integrates vasomotor mechanisms with renal processes, where vascular tone contributes to pressure buffering by modulating PR in response to sustained changes in extracellular fluid volume. The vascular system supports this through ongoing adjustments that complement renal sodium and water handling, with humoral factors like the renin-angiotensin-aldosterone system (RAAS) providing brief reinforcement to vasomotor tone during volume perturbations.^[46]^[41]

Thermoregulation

The hypothalamic thermoregulatory center, particularly the preoptic/anterior hypothalamus (PO/AH), serves as the primary integrator of thermal signals from core body temperature and skin thermoreceptors, orchestrating vasomotor responses to maintain homeostasis by modulating cutaneous blood flow for heat exchange. Warm-sensitive neurons in the PO/AH inhibit vasoconstrictor pathways and activate vasodilator systems, while cold-sensitive neurons excite sympathetic vasoconstrictor outflow via projections to the medullary raphe, a key relay for cutaneous vasomotor control.^[47] These reflex adjustments prioritize skin vessels in nonglabrous areas, where blood flow can vary dramatically to either dissipate or conserve heat without significantly impacting systemic circulation. During heat stress, active cutaneous vasodilation predominates, accounting for approximately 80% of the response through cholinergic sympathetic fibers that co-release acetylcholine (ACh) as a cotransmitter, alongside a smaller contribution (10-20%) from the withdrawal of tonic noradrenergic vasoconstrictor activity. This mechanism elevates skin blood flow up to 6-8 L/min, facilitating convective heat loss to the environment. Endothelial nitric oxide (NO) further supports sustained dilation, contributing about 30% to the vasodilatory drive, though its role is secondary to neural activation. In cold exposure, noradrenergic sympathetic activation induces cutaneous vasoconstriction, minimizing heat loss by reducing skin blood flow to below 0.5 L/min through norepinephrine release and co-transmitters acting on arteriolar smooth muscle. This response is rapidly elicited by hypothalamic cooling signals transmitted via glutamatergic projections from the rostromedial preoptic region to the medullary raphe, ensuring peripheral vasoconstriction as the initial defense against hypothermia.^[47] Vasodilation integrates closely with sweating for evaporative cooling, as cholinergic sympathetic activation to sweat glands often precedes or coincides with vasodilator outflow, allowing warmed blood in dilated vessels to be cooled by sweat before recirculation. This coordinated thermoeffector response enhances overall heat dissipation efficiency during hyperthermia.

Pathological Aspects

Menopausal Vasomotor Symptoms

Menopausal vasomotor symptoms (VMS), commonly known as hot flashes and night sweats, represent a hallmark of the menopausal transition, characterized by the sudden onset of cutaneous vasodilation and sweating. These episodes typically last 1-5 minutes and affect 75-85% of perimenopausal women, making them the most prevalent symptom during this phase.^[48]^[49] The pathophysiology of VMS stems from estrogen withdrawal during the menopausal transition, which narrows the thermoneutral zone in the hypothalamus and triggers inappropriate activation of heat-loss mechanisms, including peripheral vasodilation and sweating, even when core body temperature remains normal. This instability arises from altered neurotransmitter activity, such as increased norepinephrine and changes in serotonin signaling, leading to exaggerated sympathetic nervous system responses.^[50]^[51] Risk factors for experiencing VMS include early onset of menopause, cigarette smoking, and African American ethnicity, with the latter group reporting higher prevalence and severity compared to other racial groups. The average duration of VMS is 7-10 years, though episodes can persist longer in women with earlier symptom onset.^[52]^[53]^[54] VMS significantly impact quality of life, causing sleep disruption through frequent night sweats that fragment rest, as well as mood changes including increased anxiety and depressive symptoms often mediated by poor sleep. Additionally, the repeated sympathetic surges associated with VMS are linked to elevated cardiovascular risk, including higher incidence of hypertension and coronary heart disease.^[55]^[56]^[57]

Vasomotor Rhinitis and Vascular Dysfunctions

Vasomotor rhinitis, also known as nonallergic rhinitis, is characterized by chronic nasal symptoms such as congestion and rhinorrhea without involvement of immunoglobulin E-mediated allergic mechanisms.^[8] These symptoms are typically triggered by nonallergic irritants, including environmental factors like temperature fluctuations, humidity changes, strong odors, smoke, or even emotional stress.^[58] The underlying pathophysiology involves an autonomic nervous system imbalance, often with parasympathetic hyperactivity, leading to nasal blood vessel dilation (vasodilation) and excessive glandular secretion in the nasal mucosa.^[59] This condition accounts for approximately 20% of all rhinitis cases, making it a significant subset of nonallergic rhinitis syndromes.^[60] Beyond the nasal vasculature, vasomotor dysfunctions manifest systemically in various cardiovascular pathologies, where impaired vascular tone regulation contributes to disease progression. In atherosclerosis, endothelial impairment reduces nitric oxide (NO) bioavailability, a key vasodilator, resulting in diminished endothelium-dependent vasodilation and increased susceptibility to vasospasm.^[61] This endothelial dysfunction promotes plaque formation and instability, exacerbating arterial narrowing.^[62] In hypertension, chronic endothelial dysfunction leads to heightened vascular tone and impaired relaxation, perpetuating elevated blood pressure.^[63] Similarly, Raynaud's phenomenon involves exaggerated vasoconstriction in response to cold or stress, often due to abnormal vasomotor reactivity in peripheral arteries, causing episodic ischemia in the digits.^[64] Other vasomotor-related conditions highlight failures in vascular responsiveness. Orthostatic hypotension arises from inadequate vasoconstriction upon postural change, failing to maintain blood pressure and leading to cerebral hypoperfusion.^[65] In septic shock, profound vasodilatory failure occurs due to systemic inflammation and cytokine release, causing widespread vascular hyporesponsiveness to endogenous vasoconstrictors and refractory hypotension.^[66] Diagnosis of these vasomotor pathologies relies on targeted approaches to confirm dysfunction while excluding other causes. For vasomotor rhinitis, the process involves a detailed history of nonallergic triggers and exclusion of allergens through negative skin prick testing or serum IgE assays.^[8] In vascular dysfunctions, such as those in atherosclerosis or hypertension, flow-mediated dilation (FMD) testing via brachial artery ultrasound serves as a noninvasive measure of endothelial function, where reduced dilation indicates impaired vasomotor capacity.^[67]

References

[1]
Definition of vasomotor - NCI Dictionary of Cancer Terms
vasomotor. Listen to pronunciation. (VAY-zoh-MOH-ter). Affecting the narrowing and widening of the blood vessels. Search NCI's Dictionary of Cancer Terms.
[2]
Medical Definition of Vasomotor - RxList
Vasomotor: Relating to the nerves and muscles that cause blood vessels to constrict or dilate. Drug Categories
[3]
Vasomotor - an overview | ScienceDirect Topics
Vasomotor refers to the mechanisms that regulate the constriction and dilation of blood vessels, which are influenced by vascular smooth muscles and the ...Neuroanatomy and... · Vasomotor Function in... · Clinical Implications of...
[4]
Vasomotor Center - an overview | ScienceDirect Topics
The vasomotor center is defined as the main center for neurogenic control of vascular tone and blood pressure, located in the midbrain.
[5]
Vasomotor tone and the role of nitric oxide - PubMed
Vasomotor tone is the end result of a complex set of interactions that control relaxation and contraction of blood vessels. The critical role of nitric ...
[6]
Menopause - Gynecology and Obstetrics - MSD Manuals
Vasomotor. Hot flushes (hot flashes) and/or night sweats due to vasomotor instability affect 75 to 85% of women and usually begin before menses stop. Vasomotor ...
[7]
https://www.ncbi.nlm.nih.gov/books/NBK57142/
[8]
Evolving Mechanisms of Vascular Smooth Muscle Contraction ...
Vascular smooth muscle (VSM) is a major component of the tunica media of blood vessels, and an important regulator of vascular function. VSM contraction ...
[9]
Vascular Smooth Muscle TRPV4 (Transient Receptor Potential ...
Feb 16, 2023 · Vasomotor changes of mouse mesenteric artery were measured by wire, and pressure myography. ... tunica media of arteries caused by ...
[10]
The discovery of vasomotor nerves | Clinical Autonomic Research
The relative contribution of Claude Bernard and Charles Edouard Brown-Séquard to the discovery of vasomotor nerves is described and discussed.
[11]
Regulation of Cerebrovascular Tone - The Cerebral Circulation - NCBI
Discovered over 100 years ago by Bayliss, the myogenic response is the intrinsic property of smooth muscle to respond to changes in mechanical load or ...Missing: Starling 1894
[12]
Vascular Smooth Muscle Cell Signaling Mechanisms for Contraction ...
The EF hand Ca2+ -binding protein, calmodulin, is the primary target for elevated intracellular Ca2+. The Ca2+ -calmodulin complex is then able to activate MLCK ...
[13]
Sympathetic Neural Mechanisms in Human Cardiovascular Health ...
Sympathetic innervation of the peripheral vasculature causes vasoconstriction primarily through the action of norepinephrine at postsynaptic α-adrenergic ...
[14]
Regulation of Vascular Tone in Skeletal Muscle - NCBI - NIH
The amount of VSM contraction necessary to maintain this partially constricted state is called basal vascular or vasomotor tone [109, 110, 453]. Changes in the ...Missing: definition | Show results with:definition
[15]
Vasodilator efficacy of nitric oxide depends on mechanisms of ... - NIH
Reduction of intracellular calcium ([Ca2+]i) in smooth muscle cells (SMCs) is an important mechanism by which nitric oxide (NO) dilates blood vessels.
[16]
Physiology, Peripheral Vascular Resistance - StatPearls - NCBI - NIH
The basis for the mechanism of peripheral vascular resistance is expressed by the Hagen-Poiseuille equation: R = 8Ln/(pi*r^4). R is the resistance of blood ...
[17]
Commentary on the Special Issue on the Impact of Myogenic tone in ...
The myogenic response is an intrinsic property of the vascular smooth muscle cells in small arteries that constrict in response to elevations in transmural ...
[18]
Cellular mechanisms involved in the vascular myogenic response
The myogenic response is blood vessel contraction when pressure rises. Cellular mechanisms include altered membrane properties, cell-signaling, contractile ...
[19]
Differential Control of Sympathetic Outflow by Rostral Medulla
The rostral ventrolateral medulla (RVLM) is an important brain region involved in both resting and reflex regulation of the sympathetic nervous system.
[20]
Blood Pressure Regulation by the Rostral Ventrolateral Medulla in ...
Apr 26, 2017 · RVLM presympathetic neurons have multiple brain targets in addition to sympathetic ... baroreceptors and peripheral chemoreceptors are the ...
[21]
Central CO2 Chemoreception & Neural Mechanisms of Control
Site 2, the rostral ventrolateral medulla (RVLM), contains the main source of direct excitatory drive to the sympathetic vasomotor preganglionic neurons.
[22]
Adrenergic and Cholinergic Receptors in Blood Vessels
Most arteries and veins in the body are innervated by sympathetic adrenergic nerves, which release norepinephrine (NE) as a neurotransmitter.<|control11|><|separator|>
[23]
The crosstalk between autonomic nervous system and blood vessels
Abnormal activation of the sympathetic nerves leads to decreases in blood flow and remarkable vasoconstriction which is mediated by α-adrenoreceptors [8]. The ...
[24]
Autonomic nervous system - Knowledge @ AMBOSS
May 13, 2025 · Transmitters of the sympathetic nervous system are acetylcholine (preganglionic → postganglionic neurons) and norepinephrine (postganglionic ...Missing: co- | Show results with:co-
[25]
Neuroanatomy, Parasympathetic Nervous System - StatPearls - NCBI
In salivary glands, parasympathetic stimulation of M1 and M3 receptors leads to high-volume secretion of potassium ions, water, and amylase. In the stomach ...
[26]
Efficacy of Electrical Baroreflex Activation Is Independent of ...
Dec 2, 2019 · Previous studies suggested that the peripheral chemoreflex is tonically active in hypertensive patients and may inhibit baroreflex responses. We ...
[27]
Baroreflex control of muscle sympathetic nerve activity as a ...
The baroreflex is reset to higher pressures in hypoxia and likely contributes to the elevated sympathetic vasoconstrictor drive in hypoxia. However, it is not ...
[28]
Endothelial Nitric Oxide Synthase (eNOS) and the Cardiovascular ...
The activation and/or overexpression of eNOS allow vasodilation and regulation of systemic blood pressure [40]. Administration of heparin-binding superoxide ...Enos Dimerization And... · Enos In Cardiac Myocytes · Enos And Stroke
[29]
Physiology, Endothelin - StatPearls - NCBI Bookshelf
They are known to produce endothelin-1 (ET-1) that acts on the receptors ETA and ETB. These receptors are G-protein coupled cell-surface receptors, and ETA is ...
[30]
Control of muscle blood flow during exercise: local factors and ...
Here we analyse the role of mediators generated by skeletal muscle activity on smooth muscle relaxation in resistance vessels in vitro and in vivo.Missing: H+ | Show results with:H+
[31]
Autoregulation of Organ Blood Flow - CV Physiology
Many studies suggest that metabolic, myogenic and endothelial mechanisms are responsible for this vasodilation. As resistance decreases, blood flow ...
[32]
Physiology, Catecholamines - StatPearls - NCBI Bookshelf - NIH
Dec 11, 2024 · Both epinephrine and norepinephrine activate these receptors, but norepinephrine has a higher affinity. Triggering α1-receptors activates ...Missing: vasomotor | Show results with:vasomotor
[33]
Physiology, Renin Angiotensin System - StatPearls - NCBI Bookshelf
The renin-angiotensin-aldosterone system (RAAS) is a critical regulator of blood volume, electrolyte balance, and systemic vascular resistance.
[34]
Vasopressin-induced vasoconstriction: two concentration ... - NIH
Additionally, AVP binds to V1a receptors on vascular smooth muscle cells to induce vasoconstriction. Skin, muscle, and splanchnic arterial beds are highly ...
[35]
Atrial and Brain Natriuretic Peptides - CV Physiology
The mechanism of systemic vasodilation involves NP receptor-mediated elevations in vascular smooth muscle cGMP and attenuation of sympathetic vascular tone.
[36]
Angiotensin-(1–7) Augments Bradykinin-Induced Vasodilation by ...
Other studies showed that ACE inhibitors potentiated BK-induced vasodilation mediated by nitric oxide and enhanced cGMP production in arteries. These ...
[37]
Physiology, Systemic Vascular Resistance - StatPearls - NCBI - NIH
Jul 10, 2023 · ... mathematically as MAP = CO x TPR, where CO stands for cardiac output, and MAP stands for mean arterial pressure.[1]Missing: basal | Show results with:basal
[38]
Mechanisms involved in regulation of Systemic Blood Pressure
Vasomotor tone is the sum of the muscular forces intrinsic to the blood vessel opposing an increase in vessel diameter [6]. This is mediated by vascular smooth ...Neural Control · Vasomotor Tone · Humoral Control
[39]
Physiology, Baroreceptors - StatPearls - NCBI Bookshelf
Baroreceptor exerts control of mean arterial pressure as a negative feedback loop. Nerve impulses from arterial baroreceptors are tonically active; increases ...
[40]
Baroreflex Regulation of Heart Rate and Sympathetic Vasomotor ...
May 2, 2005 · Baroreflexes are an important mechanism by which the central nervous system controls blood pressure in response to acute challenges imposed by ...
[41]
Vasoconstrictor Reserve and Sympathetic Neural Control of ...
Oct 25, 2004 · Normally, orthostatic stress evokes compensatory vasoconstriction in skeletal muscle via an increase in sympathetic nerve traffic, which can be ...
[42]
Impaired Modulation of Sympathetic Vasoconstriction in Contracting ...
Sympathetic activation causes vasoconstriction in regions such as the renal and splanchnic circulations, which redistributes cardiac output to the exercising ...
[43]
The Sympathetic Nervous System and Hypertension
The renal body fluid feedback mechanism couples the long-term regulation of arterial pressure to extracellular volume (sodium and water) homeostasis via ...
[44]
https://www.ahajournals.org/doi/10.1161/01.cir.0000146384.91715.b5
[45]
Menopausal hot flashes: Mechanisms, endocrinology, treatment
HFs usually last for 1–5 min, with some lasting as long as an hour [1]. The median duration of symptoms is about four years, with some lasting as long as 20 ...Endocrinology Of Hot Flashes · Circadian Rhythm Of Hot... · Hot Flashes (hfs) And Sleep
[46]
Vasomotor Symptoms Across the Menopause Transition
Vasomotor symptoms occur during the MT for up to 80% of US women, but the daily frequency varies. On average, women report 4–5 hot flashes per day, although ...
[47]
Vasomotor Symptoms During Menopause: A Practical Guide on ...
Feb 14, 2023 · This review aims to summarize treatment options for bothersome vasomotor symptoms to guide clinicians caring for midlife women.Missing: definition | Show results with:definition<|control11|><|separator|>
[48]
MENOPAUSAL HOT FLASHES: MECHANISMS, ENDOCRINOLOGY ...
Taken together, these data formed the basis of our theory that elevated brain NE, in conjunction with estrogen withdrawal, are part of the etiology of HFs.1. Physiologic Events Of The... · Fig. 1 · 2. Objective Measurement Of...
[49]
Study of Women's Health Across the Nation | AJPH
Oct 10, 2011 · Many factors were related to vasomotor symptoms independent of race/ethnicity and menopausal transition status. Older age, lower education level ...
[50]
Duration of Menopausal Hot Flushes and Associated Risk Factors
The median duration of moderate to severe hot flushes was 10.2 years and was strongly associated with menopausal stage at onset.
[51]
Hot Flashes—How Long ?? - PMC - NIH
Not so, says a new study of women going through menopause. Hot flashes and night sweats last, on average, for about 7 years and may go on for 11 years or more.
[52]
Association of menopausal vasomotor symptom severity with sleep ...
Aug 25, 2023 · Greater vasomotor symptom severity was associated with more sleep disturbance, more sleep-related impairment, worse sleep quality, and greater impairment in ...
[53]
The role of sleep difficulties in the vasomotor menopausal symptoms ...
Midlife women who seek clinical help for VMS are likely to have concurrent and subsequent depressed mood, which may be largely explained by sleep difficulties.
[54]
Vasomotor Menopausal Symptoms and Risk of Cardiovascular ... - NIH
Severity rather than frequency of VMS (hot flushes and night sweats) was associated with increased risk of CVD. VMS with onset before or after menopause were ...Missing: impact disruption
[55]
Vasomotor Rhinitis - StatPearls - NCBI Bookshelf
Vasomotor rhinitis is a term often used to describe rhinitis symptoms associated with nonallergic, noninfectious triggers with no clear etiology.Missing: physiology | Show results with:physiology
[56]
Characteristics of Nonallergic Vasomotor Rhinitis - PMC
Symptoms are classically aggravated by irritant triggers such as tobacco smoke, perfumes/fragrances, and temperature or barometric pressure changes. A ...
[57]
Non-allergic rhinitis: a case report and review - PMC - PubMed Central
Vasomotor or idiopathic rhinitis (VMR) is the most commonly diagnosed form of NAR, accounting for ~60% cases in one series [5]. VMR is characterized by sporadic ...
[58]
Nonallergic Rhinitis, With a Focus on Vasomotor ... - PubMed Central
These data suggest that at least 57% of rhinitis patients have some contribution from NAR causing their rhinitis symptoms. Similar European studies have found ...
[59]
Endothelial Dysfunction: Cardiovascular Risk Factors, Therapy, and ...
Endothelial dysfunction is characterized by reduction of the bioavailability of vasodilators, particularly nitric oxide (NO), and/or an increase in endothelium- ...
[60]
Endothelial dysfunction: a marker of atherosclerotic risk
Coronary endothelial dysfunction, which is characterized by impaired NO bioavailability, may be associated with myocardial ischemia. Both physical ...
[61]
Endothelial dysfunction as a factor leading to arterial hypertension
Nov 21, 2022 · A dysfunctional endothelium contributes to the development of hypertension and further cardiovascular complications. Reduced nitric oxide (NO) ...
[62]
Raynaud's Phenomenon: A Brief Review of the Underlying ... - NIH
Nov 16, 2016 · Raynaud's phenomenon (RP) is characterized by exaggerated cold-induced vasoconstriction. This augmented vasoconstriction occurs by virtue of a reflex response ...
[63]
Orthostatic Hypotension - StatPearls - NCBI Bookshelf
Jan 17, 2025 · Orthostatic hypotension occurs due to an inadequate physiological response to postural changes. ... vasodilation, impairment of vasoconstriction ...
[64]
Advances in Vasodilatory Shock: A Concise Review - PMC
There is uncontrolled vasodilation and vascular hyporesponsiveness to endogenous vasoconstrictors, causing the failure of physiologic vasoregulatory mechanisms.
[65]
Flow-mediated dilatation - PMC - NIH
Thus, there are much data to support a link between arterial endothelial dysfunction and later advanced atherosclerotic disease and the use of FMD as a ...