Pressoreceptor Reflex

BEI is divers as the ratio between the number of sequences occurring in a given menstruum of time, and the number of blood pressure ramps, i.e., progressive increases or progressive reductions of SBP of iii or more beats.

From: Encyclopedia of Stress (Second Edition) , 2007

Baroreceptor Reflexes

Mark W. Chapleau , in Primer on the Autonomic Nervous System (Third Edition), 2012

Publisher Summary

This chapter focuses on baroreceptor reflexes, neural pathways, and effector mechanisms. The cardiopulmonary region is innervated past multiple types of mechanosensitive and chemosensitive sensory nerves that bear on autonomic and cardiovascular functions in a variety of means. Baroreceptors are not direct sensitive to blood pressure (BP), only rather are sensitive to mechanical deformation of the nerve endings during amplification of the arterial wall. Baroreflex sensitivity (BRS) for control of HR is consistently decreased in numerous pathological states including chronic hypertension, coronary avenue disease postmyocardial infarction, eye failure, diabetes mellitus, and obesity, and with aging. The potent inverse relationship between BRS and cardiovascular risk encourages targeting therapy to meliorate BRS. Baroreflexes may contribute to the do good of standard antihypertensive therapies. For example, lowering of BP of hypertensive patients by pharmacological or dietary interventions apace resets the baroreflex office bend to lower mean arterial BPs. Cholinesterase inhibitors promote increases in cardiovagal tone and BRS by increasing the concentration of the neurotransmitter acetylcholine at cholinergic synapses and sinoatrial node, and amplify cholinergic signaling in left ventricle.

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Baroreflex Failure

Jens Jordan , in Primer on the Autonomic Nervous System (Third Edition), 2012

Introduction

Baroreflexes have an of import function in curt term blood pressure level regulation. Baroreflex mechanisms may also be involved in chronic blood pressure regulation. Blood pressure level changes distend arteries, thus, eliciting carotid and aortic baroreceptor stretch. The electric signal generated in carotid and aortic baroreceptors is conveyed to medullary brainstem nuclei via the glossopharyngeal and vagus nerves where it is integrated with input from other afferents and cortical input. Efferent parasympathetic and sympathetic activities are adjusted to compensate for the change in systemic claret pressure. Thus, baroreflexes attenuate excessive swings in blood pressure and thereby maintain blood flow, particularly to the brain. Moreover, the vasculature is protected from large, potentially deleterious, blood pressure fluctuations.

Bilateral harm to afferent baroreflex structures results in baroreflex failure. Any afferent arc construction including baroreceptors, afferent neurons transmitting information from baroreceptors, or afferent brainstem nuclei may be involved. In contrast, damage to the efferent part of the baroreflex causes autonomic failure (Table 72.i). Whether or not the afferent baroreflex input must be completely lost to develop baroreflex failure is non known. In nigh baroreflex failure patients, the lesion of the afferent arc of the baroreflex seems to be associated with damage to efferent neurons in the vagus nerve. The damage results in partial or complete parasympathetic denervation of the heart ("nonselective baroreflex failure") (Fig. 72.ane). In a minority of patients, efferent parasympathetic neurons are intact ("selective baroreflex failure") (Fig. 72.one).

Table 72.1. Distinction of Baroreflex Failure and Autonomic Failure

Baroreflex Failure Autonomic Failure
Labile hypertension +++ +/−
Orthostatic hypotension +/− +++
Orthostatic hypertension ++ −
Supine hypertension +/− ++
Postprandial hypotension +/− ++
Episodic tachycardia ++ −
Bradycardic episodes ++* +/−
Hypersensitivity to vasoactive drugs +++ +++
*
Bradycardia associated with hypotension is a typical feature of malignant vagotonia due to selective baroreflex failure.

Figure 72.1. Selective baroreflex failure (meridian) contrasted to nonselective baroreflex failure (bottom). Baroreflex afferents (BA) are damaged in selective and nonselective baroreflex failure patients. Efferent sympathetic (SNS) and parasympathetic nerves (PNS) are intact in selective baroreflex failure. In nonselective baroreflex failure, efferent parasympathetic fretfulness are at least in role damaged.

 From Hashemite kingdom of jordan et al. [9].

There is a large body of literature on baroreflex part, both, in different creature species and in humans. However, the number of baroreflex failure patients reported in the literature is relatively small. The small-scale number of reported cases may propose that baroreflex failure is a rare status. Perhaps, the probability to experience bilateral damage to afferent baroreflex structures is low. An alternative explanation is that many cases of baroreflex failure go undetected.

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Autonomic Nervous Organization

Erica A. Wehrwein , Michael J. Joyner , in Handbook of Clinical Neurology, 2013

What is baroreflex sensitivity?

Baroreflex sensitivity (BRS) (also known as baroreflex gain) is used every bit a measure of autonomic command of the cardiovascular system. Mostly, it is a measure of the autonomic effector response to a given change in arterial pressure. In that location are a variety of methods used to determine BRS that are farther explored beneath (encounter Cess of baroreflex function for detailed methodology).

As an instance, when MAP is altered pharmacologically using the vasoconstrictor phenylephrine and vasodilator sodium nitroprusside, a large range of pressures can be observed. The changes in pressure, both high and low, are associated with the baroreflex counterregulation in heart rate. The heart rate responses over the wide range of pressures generated with this type of intervention are plotted equally in Figure viii.2. A sigmoidal human relationship exists and the linear portion of the curve is analyzed by regression to determine slope and BRS. A greater autumn in heart rate to a given pressure elevation is indicative of a college BRS. The BRS is low when the slope is flat such that there is a minimal heart rate response to a change in MAP (Fig. viii.2). In other words, for a given modify in MAP sensed by the baroreceptors in that location is a baroreflex-driven change in eye rate and the nature of this human relationship determines the BRS.

Fig. viii.2. Baroreflex sensitivity (BRS) (also chosen baroreflex gain). BRS is used every bit a measure of autonomic control of the cardiovascular organization. BRS is determined from the slope of the human relationship of mean arterial pressure (MAP) (systolic and diastolic arterial pressures or carotid sinus pressures can likewise be used) and center rate (or sympathetic nervus activity). The heart rate (or sympathetic nerve activity) over a range of claret pressures is plotted and analyzed by linear regression. The slope of this regression line obtained from the linear function of the curve is the BRS. The BRS is loftier when the slope is steep (solid line) such that there is a big centre rate response to a given modify in MAP. The BRS is low when the slope is apartment (dashed line) such that at that place is a minimal eye rate response to a alter in MAP.

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Cardiovascular Consequences of Obstructive Slumber Apnea

Abu Shamsuzzaman , Raouf Amin , in Principles and Practise of Pediatric Sleep Medicine (Second Edition), 2014

Baroreflex and Chemoreflex Interactions

Baroreflex activation inhibits both ventilatory and vasoconstrictor responses to peripheral chemoreflex stimulation. 29 Increased BP activates arterial baroreceptors and causes bradycardia. 30 Chemoreflex activation in the setting of apnea also elicits bradycardia. The bradycardic response is attenuated when chemoreflex activation and apnea occur in a setting of increased baroreflex activation. Thus, the arterial baroreflex inhibits not only the chemoreflex-mediated sympathetic vasoconstrictor response, merely also the vagal bradycardic response. 30 The normal buffering influence of the baroreflex may be diminished in patients with SDB, 30 resulting in excessive potentiation of chemoreflex sensitivity with consequent exaggerated sympathetic activation and/or brady-dysrhythmias during hypoxemia and apnea. Interaction of chemoreceptor and baroreceptor reflexes during repeated episodes of OSA could be a mechanism for increased BP and promoting hypertension in OSA. 31 Decreased baroreflex sensitivity is a potential machinery of BP elevation in children with SDB. 32 Bear witness of abnormal baroreflex function in children with SDB volition be discussed in the section on SDB-related cardiac dysfunction.

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Sympathetic Innervation and Cardiac Arrhythmias

David Filgueiras-Rama , in Cardiac Electrophysiology: From Cell to Bedside (Seventh Edition), 2018

Baroreflex Sensitivity

Baroreceptor reflexes tin can exist modulated by cardiac afferent sympathetic activity activated by mechanical and chemical stimuli. 68 Baroreflex sensitivity represents an index of autonomic input to the sinus node and is measured by the reflex changes in R-R interval in response to induced changes in claret force per unit area. It is commonly measured by characterizing the magnitude of induced bradycardia in response to a pressor challenge (e.g., phenylephrine). A reduction in baroreflex control of heart charge per unit has been consistently reported in hypertension, diabetes, coronary artery disease, myocardial infarction, and heart failure. 69 Rather than a risk cistron, baroreflex sensitivity assessed by the phenylephrine exam has been shown to exist a modifiable risk factor 70 ; thus an improved prognosis was observed for those patients in whom exercise preparation was able to induce a notable increase in baroreflex sensitivity.

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Arterial Baroreflex*

Thousand. Parati , ... G. Mancia , in Encyclopedia of Stress (Second Edition), 2007

The arterial baroreflex plays a pivotal part in human cardiovascular physiology and pathophysiology. Its part tin be assessed in humans by different methods, either in a laboratory environs or nether spontaneous daily life conditions, which may have both pros and cons in relation to the baroreflex assessment conditions. While laboratory methods accept largely contributed to our present cognition of arterial baroreflex part in humans, modernistic techniques for spontaneous baroreflex analysis take more recently provided us with a much deeper insight into the features of daily life baroreflex role. The recent bear witness on the prognostic relevance of the sensitivity of baroreflex center rate modulation obtained in myocardial infarction patients, in patients with congestive eye failure or stroke, and in patients with diabetes has increased the involvement towards baroreflex analysis in humans.

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Autonomic Failure

East.M. Garland , D. Robertson , in Encyclopedia of Neuroscience, 2009

Clinical Manifestations

Baroreflex failure, a rare disorder, is a issue of damage along the baroreflex arc at the baroreceptors, along the glossopharyngeal or vagal fretfulness, or in the brain stem nuclei. It is more often than not a result of cervix surgery, caput or cervix irradiation for carcinoma, brain stem lesions, or bilateral carotid body tumors.

Acute break of the baroreflex arc, with damage isolated to the afferent limb, may exist associated with astringent, sustained hypertension, tachycardia, and headache. Diaphoresis and apnea may occur, especially in the showtime 48   h postoperatively. Labile, episodic hypertension (volatile hypertension), on the other hand, is oftentimes seen in patients who develop baroreflex failure gradually or during a more chronic phase of the disorder. Surges in blood pressure are elicited past mental or physical stress, during which sympathetic outflow is increased. These patients experience sensations of warmth or flushing, dizziness or calorie-free-headedness, palpitations, headache, and diaphoresis. Tremulousness, anxiety, and irritability may besides exist nowadays. In patients with baroreflex failure, periods of volatile hypertension can be interrupted by hypotensive episodes, peculiarly during periods of quiet, sedation, or sleep, when sympathetic outflow is macerated.

In some cases of baroreflex failure, with interruption of efferent vagal function, tachycardia is provoked by mild sympathetic activation. In other patients, with selective baroreflex failure (Jordan syndrome), the lesion is in the afferent input from the carotid sinus to the nucleus tractus solitarii, and efferent sympathetic and parasympathetic output remains intact. Malignant vagotonia with hypotension, bradycardia, and asystole characterize selective baroreflex failure. Accompanying symptoms include fatigue and dizziness, with possible syncope. Plasma NE levels in baroreflex failure tend to parallel the claret pressure changes. During periods of relatively low sympathetic activity, NE may be normal (111–360   pg   ml−1 (0.66–two.13   nM)). During hypertensive-tachycardic episodes, plasma NE may ascent to levels equally high as 2260   pg   ml−ane (13.36   nM).

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Neuronal Hormones and the Sympathetic/Parasympathetic Regulation of the Centre

Grand.J. Ranek , ... A. Lymperopoulos , in Endocrinology of the Center in Health and Affliction, 2017

Physiology and Pathophysiology of Cardiovascular Function Involving the Autonomic System: Pregnancy and the Baroreflex

The baroreceptor reflex is the mechanism by which arterial pressure level is maintained through autonomic regulation inside a prepare range, although this set range can shift during physiological and pathophysiological atmospheric condition (Fig. eight.viii). During pregnancy, the cardiovascular system undergoes pregnant changes to appropriately serve the developing fetus. In early gestation, the female parent's blood volume and cardiac output increases by xxx–fifty%; nevertheless, there is also a reduction in arterial pressure. Reduced arterial pressure level is due to suppression of the baroreflex response, which decreases systemic vascular resistance. The baroreflex dysfunction that occurs during pregnancy is due to reduced sympathetic modulation of the vasculature, thus limiting the response to vasoconstriction and increased arterial pressure. 89,xc The machinery for the macerated baroreflex response is attributed to (1) reduced insulin interim in the encephalon that normally supports the baroreflex and (2) increased levels of the neurosteroid progesterone metabolite, 3α-hydroxy-dihydroprogesterone (3α-OH-DHP). 91

Effigy 8.8. A schematic overview of the baroreflex response.

The baroreflex response is mediated by afferent and efferent innervations to and from the brainstem. Afferent fretfulness for the baroreflex response terminate in the nucleus tractus solitarius, project to the caudal ventrolateral medulla that projects to the rostral ventrolateral medulla (RVLM). Efferents then project to the baroreflex receptors. During pregnancy, there is a reduction of insulin action, which facilitates the placental transfer of glucose to the fetus by increasing circulating glucose levels. Insulin enhances the baroreflex response, thus when insulin is decreased the baroreflex response is impaired. The concentration of the neurosteroid, 3α-OH-DHP in the blood, increases during pregnancy. 3α-OH-DHP acts on the RVLM to inhibit efferent signaling originating in the RVLM. 91 In plow, the diminished baroreflex response signals dorsum to the vasculature to increase arterial pressure. Collectively, these mechanisms suppress the baroreflex response during pregnancy.

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Bionic Baroreflex

Takayuki Sato , ... Kenji Sunagawa , in Primer on the Autonomic Nervous Arrangement (Third Edition), 2012

Introduction

The arterial baroreflex is the most important negative feedback system to suppress rapid daily disturbances in arterial pressure level [ane]. Therefore, in patients with autonomic failure with dysfunctional baroreflex command of arterial pressure, the elementary human activity of standing would crusade a fall in arterial pressure, reducing perfusion of the brain, and resulting potentially in loss of consciousness. The functional restoration of the arterial baroreflex is essential in numerous patients groups (e.g., those with autonomic failure) for maintaining consciousness and a level of life quality.

In patients with central baroreflex failure such as baroreceptor deafferentation, Shy–Drager syndrome, and spinal cord injuries, peripheral sympathetic nerves remain functional but are not controlled by the encephalon. A novel therapeutic strategy has been proposed to use a bionic baroreflex system (Bbs) with a neural interface to control arterial force per unit area [2,3]. A bionic system is an artificial device for the functional replacement of a failed physiological organisation. Information technology is should be able to mimic its static and dynamic characteristics. In the proposed BBS (Fig. 139.ane), arterial pressure is sensed via a micromanometer placed in the aortic arch, and fed into a computer that functions equally an artificial vasomotor center. Based upon measured changes in arterial pressure level, the artificial vasomotor center generates commands signals that trigger an electrical stimulator to provide a stimulus of the appropriate frequency to vasomotor sympathetic fretfulness. The Bbs has been able to revitalize baroreflex role in an animal model of central baroreflex failure.

Figure 139.1. Primal baroreflex failure and its functional replacement by a bionic baroreflex system.

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A Study of Cardiac Function, Atherosclerosis, and Arrhythmogenicity

U. Nussinovitch , ... 1000. Malik , in The Heart in Rheumatic, Autoimmune and Inflammatory Diseases, 2017

7.5 Baroreflex Sensitivity

The baroreflex arrangement (BRS) plays a pivotal part in the regulation of blood pressure and eye rate. Its malfunction is associated with adverse cardiovascular outcomes. Several interventions known to improve the BRS (ie, concrete activeness and β-adrenergic antagonists) may also improve prognosis. In that location are many unlike ways to trigger a baroreflex response including carotid sinus massage or electric stimulation of carotid sinus fretfulness, the Valsalva maneuver and head-upwards tilting, lower body negative pressure awarding, intravenous bolus injection of vasoactive agents, and other techniques [188]. Unlike approaches include the application of increased or reduced cervix pressure using a neck bedchamber device.

Phenylephrine is an instance of a vasopressor (α-adrenergic) that is clinically used to elicit the BRS due to its express direct cardiac effects. Information technology has replaced the infusion of angiotensin Ii used during the 1960s. Heart-rate and blood-pressure values are measured simultaneously and the BRS is calculated based on the ratio between average blood-pressure changes and the average change of the RR interval (bold a linear regression) during a prolonged infusion of phenylephrine (50–200   μg) or sodium nitroprusside (as a vasodepressor) [189]. An increase of systolic claret pressure by 15–40   mmH is obligatory in gild to perform the test [190].

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