Disease relevance of Pressoreceptors

• ANF could facilitate hypotension and natriuresis in humans by attenuating the reflex sympathetic response to baroreceptor deactivation [1].
• BACKGROUND: The purpose of this study was to test whether increased brain "ouabain" contributes to impairment of both arterial and cardiopulmonary baroreceptor reflexes in congestive heart failure (CHF) [2].
• Comparison between noninvasive indices of baroreceptor sensitivity and the phenylephrine method in post-myocardial infarction patients [3].
• These results suggest an important role for central epinephrine in regulating the peripheral sympathoadrenomedullary and the baroreceptor reflex activity, particularly when the maintenance of the high blood pressure is not renin-dependent [4].
• Relative roles of cardiac and arterial baroreceptors in vasopressin regulation during hemorrhage in conscious dogs [5].

Psychiatry related information on Pressoreceptors

• Effects of PRES baroreceptor stimulation on thermal and mechanical pain threshold in borderline hypertensives and normotensives [6].
• A group (N = 8) of restrained, baroreceptor denervated rats and a sham-operated-control group (n = 8) received discriminated classical conditioning consisting of 30 reinforced trials in which a CS+ was paired with an electric shock US and 30 non-reinforced trials in which a different CS (CS-) was presented alone [7].
• In a sample of 96 healthy, normotensive men and women, amount of pain-reduction produced by baroreceptor stimulation predicted an increase in resting BP 20 months later: the increase was proportional to self-assessed daily life stress [8].

High impact information on Pressoreceptors

• Blood volume expansion acts not only directly on the heart, by stretch of atrial myocytes to increase the release of ANP, but also on the brain ANPergic neurons through afferent inputs from baroreceptors [9].
• L-Glutamate may be the neurotransmitter of afferent nerve fibers from arterial baroreceptors [10].
• Like their endocrine and neural counterparts, these behaviors are under the control of both excitatory and inhibitory influences arising from changes in osmolality, endocrine factors such as angiotensin and aldosterone, and neural signals from low and high pressure baroreceptors [11].
• Baroreceptor regulation of vasopressin and renin secretion: low-pressure versus high-pressure receptors [12].
• Furthermore, the evidence suggests that it is the sudden unloading of arterial baroreceptors that triggers the surge in AVP secretion and not signals from cardiac receptors [12].

Chemical compound and disease context of Pressoreceptors

• Cardiovascular and neurohumoral postural responses and baroreceptor abnormalities during a course of adjunctive vasodilator therapy with felodipine for congestive heart failure [13].
• The baroreceptor fibers that were spontaneously active at low pressures were also chemically sensitive: discharge rate was increased by 5-hydroxytryptamine (10 fibers, p less than 0.01), nicotine (10 fibers, p less than 0.01), or hypercapnia (13 fibers, p less than 0.001) [14].
• The hemodynamic effects of clonidine were studied in four patients with sever idiopathic orthostatic hypotension and one patient with baroreceptor dysfunction [15].
• Hypotension and reflex tachycardia were observed in all patients during the delayed phase (15 to 60 s after adenosine injection), suggesting baroreceptor unloading [16].
• To assess the effects of ephedrine on cardiac autonomic control, baroreceptor reflex sensitivity (BRS), heart rate (HR) variability, HR response to acute myocardial ischemia, and resting catecholamines were measured before and after ephedrine [17].

Biological context of Pressoreceptors

• On an interdialysis day, both groups of patients increased vascular resistance normally during unloading of cardiopulmonary baroreceptors with lower body negative pressure and increased heart rate normally during unloading of arterial baroreceptors with infusion of nitroprusside [18].
• Baroreflex control was calculated from the slope of the regression correlating SAP to succeeding HI for PE alone (carotid and aortic baroreceptor activation) and for PE plus superimposed dynamic NP at levels equal to the increases in SAP (aortic baroreceptor activation) [19].
• The unloading of cardiopulmonary baroreceptors during upright tilt was substantial and about equal during both treatment courses, but the pulse pressure was maintained during the placebo and decreased during the felodipine period [13].
• We hypothesize that the effects are mediated by rapid, direct vasodilation induced by CRH that decreases baroreceptor input to the brain stem, leading to a rapid release of AVP that induces the antidiuresis by direct action on the V(2)Rs in the kidney [20].
• In conscious dogs, but not in rats, the fall of cardiac output is mediated by AVP stimulation of baroreceptor reflex pathways [21].

Anatomical context of Pressoreceptors

• Neck pressure (NP) was applied during PE infusion to counter the increase in transmural carotid sinus pressure, thus leaving only aortic baroreceptors stimulated by the increase in arterial pressure [19].
• The findings are consistent with the hypothesis that baroreceptor activation of the central nervous system by BVE stimulates the release of oxytocin from the neurohypophysis [22].
• The results suggest that prostaglandins (e.g., PGI2) released from endothelium contribute in a paracrine manner to activation of baroreceptors during increases in arterial pressure [23].
• It is proposed that the excitatory action of norepinephrine is independent of smooth muscle activity, and is mediated by activation of alpha 1-adrenergic receptors located on the aortic baroreceptor nerve endings [24].
• Following microinjection into the nucleus tractus solitarius (NTS), the effects of glutamate on the baroreceptor reflex are poorly antagonized by kynurenic acid and DL-2-amino-5-phosphonovaleric acid, suggesting the possible involvement of metabotropic glutamate receptors in this response [25].

Associations of Pressoreceptors with chemical compounds

• Animal studies suggest that cocaine not only blocks norepinephrine reuptake peripherally but also inhibits the baroreceptors, thereby reflexively increasing sympathetic nerve discharge [26].
• This appears to be due to decreased formation of prostacyclin rather than decreased sensitivity of the baroreceptors to prostacyclin [27].
• Inhibition of the endogenous formation of prostanoids with intrasinus administration of indomethacin (50 microM) decreased baroreceptor activity in normotensive (P less than 0.05) but not in hypertensive rabbits over a wide range of pressures [27].
• In five dogs with vagi intact, carotid sinuses isolated and held at a pressure of 100 mmHg, and aortic baroreceptors denervated, administration of lidocaine (2.5 mg/kg followed by 200 micrograms/kg per min) decreased renal nerve activity to 71 +/- 8% of control [28].
• PE increased mean arterial pressure (MAP) by 13 +/- 2 mmHg (mean +/- SEM; n = 10) and thus stimulated both carotid and aortic baroreceptors [19].

Gene context of Pressoreceptors

• Disruption of the Hoxa3 homeobox gene results in anomalies of the carotid artery system and the arterial baroreceptors [29].
• 3. With respect to baroreceptor reflex actions, it is clear that endogenous AngII impairs the gain for operation of the baroreceptor reflex, because AT1 receptor antagonists facilitate reflex function [30].
• Non-osmotic arginine vasopressin (AVP) release and biosynthesis have been shown to be increased during chronic cardiac failure (CHF) and baroreceptors pathways have been demonstrated to play a major role in this non-osmotic stimulation of AVP [31].
• The results support calcium-mediated renin stimulating properties for PTHrP, via PTH receptors, independently from baroreceptors, macula densa and prostaglandins [32].
• Effect of aortic baroreceptor deafferentation on plasma vasopressin and oxytocin in the conscious rat [33].

Analytical, diagnostic and therapeutic context of Pressoreceptors

• Since the cardiovascular responses of KA are similar to those produced by microinjection into NTS of the amino acid neurotransmitter glutamic acid, the study adds further support to the hypothesis that L-glutamate is the neurotransmitter released by baroreceptor afferent nerves [34].
• The relationship between the pulse interval (PI) and the systolic arterial blood pressure (SAP) following an intravenous injection of methoxamine was used to evaluate the sensitivity of the baroreceptor reflex in intact conscious dogs [35].
• Substance P, even at high concentrations, was less effective than atrial natriuretic factor in reducing phenylephrine constriction and in altering baroreceptor discharge [36].
• Forearm vasoconstrictor (plethysmography) and muscle sympathetic nerve activity responses to sustained handgrip were measured during cardiopulmonary baroreceptor deactivation (lower body negative pressure, n = 8) and activation (volume expansion, n = 8) [37].
• The vasopressin and oxytocin responses to hypertonic saline were greater after baroreceptor denervation [38].

References