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Frontiers in Bioscience (Landmark... Jan 2010Human thermoregulatory control during heat stress has been studied at rest, during exercise and more recently during exercise recovery. Heat balance in the body is... (Review)
Review
Human thermoregulatory control during heat stress has been studied at rest, during exercise and more recently during exercise recovery. Heat balance in the body is maintained by changes in the rate of heat loss via adjustments in skin blood flow and sweating. Independent of thermal control, the actions of nonthermal factors have important consequences in the control of heat loss responses during and following exercise. While the effect of these nonthermal factors is largely considered to be an inhibitory or excitatory stimulus which displaces the set-point about which temperature is regulated, their effects on human thermoregulatory control are far reaching. Many factors can affect the relative contribution of thermal and nonthermal influences to heat balance including exercise intensity, hemodynamic status, and the level of hyperthermia imposed. This review will characterize the physiological responses associated with heat stress and discuss the thermal and nonthermal influences on sweating and skin blood flow in humans. Further, recent calorimetric evidence for the understanding of thermal and nonthermal contributions to human heat balance will also be discussed.
Topics: Animals; Body Temperature; Body Temperature Regulation; Energy Metabolism; Exercise; Humans; Models, Biological; Pressoreceptors; Skin; Sweating
PubMed: 20036820
DOI: 10.2741/3620 -
Medical Science Monitor : International... Jan 2010Hypertension is a multifactorial disease associated with significant morbidity. Increased sympathetic nervous system activity has been noted as an important etiologic... (Review)
Review
Hypertension is a multifactorial disease associated with significant morbidity. Increased sympathetic nervous system activity has been noted as an important etiologic factor and is, in part, regulated by afferent input arising from arterial and cardiopulmonary baroreceptors, activation of which causes inhibition of sympathetic output. It was thought for many years that baroreceptors control only short-term blood pressure changes, a conclusion stemming from observations in sinoaortic denervation (SAD) animal models and the phenomenon of rapid baroreceptor resetting, also seen in animal models. Newer observations, however, indicate that SAD is rather imperfect and resetting is rarely complete. Recent studies reveal that baroreceptors control sympathetic output on a more long-term basis and participate in fluid volume regulation by the kidney, and thus have the potential to adjust blood pressure chronically. Importantly, these findings are consistent with studies and observations in humans. Meanwhile, a model of electrical stimulation of the carotid sinus has been developed and successfully tested in animals. Following these encouraging results human trials to evaluate the clinical application of electrical carotid sinus manipulation in the treatment of systemic hypertension have commenced, and results so far indicate that this represents an exciting potential tool in the clinician's armament against chronic arterial hypertension.
Topics: Animals; Blood Pressure; Carotid Sinus; Electric Stimulation; Humans; Hypertension; Models, Biological; Pressoreceptors; Sympathetic Nervous System; Water-Electrolyte Balance
PubMed: 20037502
DOI: No ID Found -
Cardiovascular Toxicology Jan 2015The body responds to environmental stressors by triggering autonomic reflexes in the pulmonary receptors, baroreceptors, and chemoreceptors to maintain homeostasis.... (Review)
Review
The body responds to environmental stressors by triggering autonomic reflexes in the pulmonary receptors, baroreceptors, and chemoreceptors to maintain homeostasis. Numerous studies have shown that exposure to various gases and airborne particles can alter the functional outcome of these reflexes, particularly with respect to the cardiovascular system. Modulation of autonomic neural input to the heart and vasculature following direct activation of sensory nerves in the respiratory system, elicitation of oxidative stress and inflammation, or through other mechanisms is one of the primary ways that exposure to air pollution affects normal cardiovascular function. Any homeostatic process that utilizes the autonomic nervous system to regulate organ function might be affected. Thus, air pollution and other inhaled environmental irritants have the potential to alter both local airway function and baro- and chemoreflex responses, which modulate autonomic control of blood pressure and detect concentrations of key gases in the body. While each of these reflex pathways causes distinct responses, the systems are heavily integrated and communicate through overlapping regions of the brainstem to cause global effects. This short review summarizes the function of major pulmonary sensory receptors, baroreceptors, and carotid body chemoreceptors and discusses the impacts of air pollution exposure on these systems.
Topics: Air Pollution; Autonomic Nervous System; Cardiovascular System; Chemoreceptor Cells; Heart Rate; Humans; Lung; Pressoreceptors; Respiratory Physiological Phenomena; Sensory Receptor Cells
PubMed: 25123706
DOI: 10.1007/s12012-014-9272-0 -
Circulation Research Jul 2021
Topics: Blood Pressure; Kidney; Pressoreceptors; Renin
PubMed: 34236885
DOI: 10.1161/CIRCRESAHA.121.319559 -
Physiology (Bethesda, Md.) Mar 2015Because of resetting, a role for baroreflexes in long-term control of arterial pressure has been commonly dismissed in the past. However, in recent years, this... (Review)
Review
Because of resetting, a role for baroreflexes in long-term control of arterial pressure has been commonly dismissed in the past. However, in recent years, this perspective has changed. Novel approaches for determining chronic neurohormonal and cardiovascular responses to natural variations in baroreceptor activity and to electrical stimulation of the carotid baroreflex indicate incomplete resetting and sustained responses that lead to long-term alterations in sympathetic activity and arterial pressure.
Topics: Animals; Antihypertensive Agents; Arterial Pressure; Baroreflex; Cardiovascular System; Homeostasis; Humans; Hypertension; Mechanotransduction, Cellular; Models, Cardiovascular; Obesity; Pressoreceptors; Renin-Angiotensin System; Time Factors
PubMed: 25729060
DOI: 10.1152/physiol.00035.2014 -
Journal of the American Society of... Jun 2019
Review
Topics: Animals; Humans; Ion Channels; Mechanotransduction, Cellular; Mice; Pressoreceptors; Sensitivity and Specificity
PubMed: 31043433
DOI: 10.1681/ASN.2019020160 -
Cell Reports Nov 2019Soohong et al. (2019) reveal a class of vagal afferents-defined by Piezo2 expression-that innervate the aorta and function to sense blood pressure fluctuations. Their...
Soohong et al. (2019) reveal a class of vagal afferents-defined by Piezo2 expression-that innervate the aorta and function to sense blood pressure fluctuations. Their study describes the morphologies and role of these neurons in vascular regulation.
Topics: Animals; Aorta; Baroreflex; Blood Pressure; Hoof and Claw; Pressoreceptors
PubMed: 31747586
DOI: 10.1016/j.celrep.2019.11.031 -
Experimental Physiology Jan 2012This report summarizes work concerning the exercise pressor reflex performed in my laboratory over the past 20 years or so. It is part of a symposium held to celebrate... (Review)
Review
This report summarizes work concerning the exercise pressor reflex performed in my laboratory over the past 20 years or so. It is part of a symposium held to celebrate the 40th anniversary of two publications by Dr Jere Mitchell that appeared in The Journal of Physiology. For the most part, this report concerns itself with the discharge properties of group III and IV muscle afferents. Particular attention has been paid to their responses to arterial injection of putative metabolic byproducts of muscular contraction as well as their responses to both static contraction and dynamic exercise.
Topics: Animals; Muscle Contraction; Muscle, Skeletal; Physical Conditioning, Animal; Pressoreceptors; Reflex
PubMed: 22058166
DOI: 10.1113/expphysiol.2011.057539 -
The Journal of Physiology Apr 19681. The carotid body and the carotid nerve were removed from anaesthetized cats and placed in a small Perspex channel through which Locke solution (at various pH values...
1. The carotid body and the carotid nerve were removed from anaesthetized cats and placed in a small Perspex channel through which Locke solution (at various pH values and usually equilibrated with 50% O(2) in N(2)) was allowed to flow. The glomus was immersed in the flowing solution while the nerve was lifted into oil covering the saline. Sensory discharges were recorded from the nerve and their frequency was used as an index of receptor activity. At times, a small segment of carotid artery, containing pressoreceptor endings, was removed together with the glomus. In this case, pressoreceptor discharges were recorded from the nerve.2. The amplitude of either chemo- or pressoreceptor discharges was not changed by strong acid solutions. Acid decreased the frequency of the baroreceptor discharges only when pH fell to less than 4.0. Solutions at low pH increased the chemosensory discharge, but acid depressed the increased chemoreceptor discharge elicited by KCl. These experiments indicated that H(+) ions probably acted as membrane ;stabilizers' without depolarizing either the nerve fibres or endings.3. Acid solutions increased the action of acetylcholine chloride (AChCl) (100-200 mug) on chemoreceptors. This effect probably was due either to inactivation of tissue cholinesterase or to enhanced sensitivity of the sensory endings to ACh.4. Choline chloride (10(-3)M), which favours ACh synthesis, protected the preparation against decay during prolonged experimentation. Hemicholinium-3 (HC-3), which blocks ACh synthesis in low concentrations (10(-5)M), depressed the chemosensory response to acid and to hypoxia when such stimuli were applied repeatedly. This concentration of HC-3 did not change effects of applied ACh.5. Substances which affect ACh release markedly changed the chemoreceptor discharge increase induced by acidity and other forms of stimulation. In the absence of Ca(2+), acid, anoxia, and interruption of flow provoked receptor depression while receptor excitation induced by ACh and KCl persisted. All stimuli excited and showed increased effectiveness as the Ca(2+) concentration was raised, but their effects declined as Ca(2+) was increased above normal values. Mg(2+) ions depressed the chemoreceptor effects induced by all these stimuli. The action of Mg(2+) was not due entirely to nerve ending block. Morphine sulphate (which decreases ACh release in other structures) also depressed the receptor response to acid and flow interruption.6. Cholinergic blocking agents such as mecamylamine, hexamethonium, atropine, dihydro-beta-erithroidine (DHE), HC-3 (10(-4)M), choline and acetylcholine (in combination with choline) depressed the effects of acid and ACh on the chemoreceptors. The effect induced by interruption of flow was depressed only by mecamylamine and DHE.7. Agents which affect the fate of released ACh, such as acetylcholinesterase and eserine salicylate, did not affect clearly the response of chemoreceptors to acid.8. The results suggest that acid stimulates chemoreceptor fibres through an indirect mechanism, viz. through increased release and/or decreased destruction of a presynaptic transmitter from the glomus cell. This transmitter is probably ACh (see following paper, Eyzaguirre & Zapata, 1968).
Topics: Acetylcholine; Acetylcholinesterase; Action Potentials; Animals; Atropine; Calcium; Carotid Body; Cats; Chemoreceptor Cells; Choline; Hexamethonium Compounds; Hydrogen-Ion Concentration; Hypoxia; Magnesium; Mecamylamine; Membrane Potentials; Methods; Morphine; Parasympatholytics; Perfusion; Physostigmine; Potassium; Pressoreceptors; Succinylcholine; Synaptic Transmission
PubMed: 4296975
DOI: 10.1113/jphysiol.1968.sp008474 -
Life Science Alliance Mar 2023Baroreceptors are nerve endings located in the adventitia of the carotid sinus and aortic arch. They act as a mechanoelectrical transducer that can sense the tension...
Baroreceptors are nerve endings located in the adventitia of the carotid sinus and aortic arch. They act as a mechanoelectrical transducer that can sense the tension stimulation exerted on the blood vessel wall by the rise in blood pressure and transduce the mechanical force into discharge of the nerve endings. However, the molecular identity of mechanical signal transduction from the vessel wall to the baroreceptor is not clear. We discovered that exogenous integrin ligands, such as RGD, IKVAV, YIGSR, PHSRN, and KNEED, could restrain pressure-dependent discharge of the aortic nerve in a dose-dependent and reversible manner. Perfusion of RGD at the baroreceptor site in vivo can block the baroreceptor reflex. An immunohistochemistry study showed the binding of exogenous RGD to the nerve endings under the adventitia of the rat aortic arch, which may competitively block the binding of integrins to ligand motifs in extracellular matrix. These findings suggest that connection of integrins with extracellular matrix plays an important role in the mechanical coupling process between vessel walls and arterial baroreceptors.
Topics: Rats; Animals; Pressoreceptors; Mechanotransduction, Cellular; Aorta; Arteries
PubMed: 36625204
DOI: 10.26508/lsa.202201785