A Mathematical Model to Assess Changes in the Baroreceptor Reflex

Kent, B; Drane, J. Wanzer; Blumenstein, B.B.; Manning, Janet R.

doi:10.1159/000169528

Cited by 371 publications

(293 citation statements)

References 17 publications

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“…Data for the MAP-RSNA or MAP-HR relations during increases and decreases in MAP were fitted to a sigmoid logistic function curve. The equation used for the data analysis was based on the following mathematical model: 15,18 RSNA or HRϭP 1 /{1ϩexp[P 2 (MAP-P 3 )]}ϩP 4 In this equation, P 1 is the range between the upper and lower plateau; P 2 , a range-independent measure of slope or normalized gain; P 3 , the blood pressure at the midpoint of the logistic function curve; and P 4 , the lower plateau. Data were fit to the logistic function curve using a nonlinear regression program in the Statistical Analysis System (NLIN procedure, SAS Institute).…”

Section: Effects Of Icv Infusion Of Ghrelin On Baroreceptor Reflexmentioning

confidence: 99%

Central Ghrelin Modulates Sympathetic Activity in Conscious Rabbits

et al. 2002

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Abstract-Ghrelin is an orexigenic peptide originally isolated from the stomach. Intravenous administration of ghrelin has been shown to elicit a decrease in arterial pressure without a significant change in heart rate (HR), suggesting that ghrelin may act on the central nervous system to modulate sympathetic activity. The aim of the present study was to determine the central effects of ghrelin on cardiovascular and sympathetic responses in conscious rabbits. Key Words: baroreceptors Ⅲ blood pressure Ⅲ central nervous system Ⅲ ghrelin Ⅲ nervous system, sympathetic renal G hrelin, an acylated 28-residue peptide originally isolated from the rat stomach, is an endogenous ligand for the growth hormone (GH) secretagogue receptor. 1,2 Although ghrelin is likely to regulate pituitary GH secretion along with GH-releasing hormone and somatostatin, 2,3 GH secretagogue receptors have also been identified in hypothalamic neurons and in the brainstem. 4,5 Intracerebroventricular (ICV) administration of ghrelin has been shown to generate a dose-dependent increase in food intake and body weight, 6,7 suggesting that ghrelin participates in the regulation of food intake and GH secretion. Furthermore, ICV administration of ghrelin has been shown to increase plasma vasopressin level without a significant change in arterial pressure in conscious rats. 8 It has also been reported that intravenous injection of human ghrelin elicits a decrease in blood pressure without an increase in heart rate (HR) in healthy men. 9 In addition, plasma ghrelin concentration is increased in patients with cachexia associated with chronic heart failure. 10 These previous findings suggest that ghrelin may participate not only in feeding behavior but also in cardiovascular and sympathetic regulation. Although ghrelin has been reported to have a vasodilatory effect in humans, 11 the underlying mechanisms of depressor response induced by intravenous injection of ghrelin have not yet been determined. Because the depressor response was not accompanied by tachycardia, it is likely that mechanisms other than direct vasodilating effects, at least in part, are involved in this depressor response. To clarify the mechanisms for this depressor response, the effects of ghrelin on sympathetic activity and on the baroreceptor reflex should be determined. We hypothesized that intravenous administration of ghrelin acts at the central nervous system to modulate the sympathetic nervous system, resulting in a decrease in arterial pressure without tachycardia. Accordingly, in the present study, we focused on the central effect of ghrelin on sympathetic activity and baroreceptor reflex. To evaluate the sympathetic nervous system precisely, the present study was conducted on conscious rabbits with direct recording of renal sympathetic nerve activity (RSNA), because the sympathetic nervous system and baroreceptor reflex are greatly affected by anesthesia. 12,13

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Section: Effects Of Icv Infusion Of Ghrelin On Baroreceptor Reflexmentioning

confidence: 99%

Central Ghrelin Modulates Sympathetic Activity in Conscious Rabbits

et al. 2002

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“…1) was assessed by a non-linear regression technique with a mod ified Marquardt algorithm, which fitted the data on a sigmoid logistic curve (11). Multiple comparisons between mean values before and after ischemia were performed using one-way analysis of variance followed by a control significant-difference method (Dunnett's t test).…”

Section: Statisticsmentioning

confidence: 99%

Difference between Halothane and Barbiturate Anesthesia in the Influence of Cerebral Ischemia on the Vagal Baroreflex in Dogs.

Kurihara

Kato

1992

Jpn.J.Pharmacol

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ABSTRACT-In halothane-anesthetized dogs, a decrease in baroreflex sensitivity (BRS) of approximately 20% was observed during the reperfusion period following 5 min global cerebral ischemia. When compared with our previous study on animals under pentobarbital anesthesia, the extent of the decrease in BRS was smaller and apparently more severe ischemia was necessary to damage the vagal component of the baroreflex. Substitution of halothane with pentobarbital during the reperfusion period failed to affect either BRS or the ratio of the vagal component. In another group, pre and post-ischemic measurements of BRS was performed under halothane anes thesia, but the ischemic insult was given under thiopental anesthesia. In these animals, the extent of decrease in BRS (about 50%) was greater than that in animals subjected to ischemia under halothane anesthesia. The present results suggest that the anesthe tics used during the ischemic insult may affect the extent of post-ischemic dysfunction of the baroreflex. The vagal component of the baroreflex may be more resistant to ischemia under halothane anesthesia than under barbiturate anesthesia.

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“…The maximum slope (maximum gain) was calculated as (P1 ϫ P2)/P4. The threshold pressure (Pth, lowest pressure that produces a significant decline in HR) and saturation pressure (pressure necessary to achieve maximal inhibition of HR) were calculated from the third derivative of the equation (16). The data were analyzed using a computer-based program (SigmaPlot2000, SPSS).…”

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confidence: 99%

Differential modulation of baroreflex control of heart rate by neuron- vs. glia-derived angiotensin II

Sakai

Chapleau

Morimoto

et al. 2004

Physiological Genomics

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. Differential modulation of baroreflex control of heart rate by neuron-vs. glia-derived angiotensin II. Physiol Genomics 20: 66-72, 2004. First published October 5, 2004 doi: 10.1152/physiolgenomics.00168.2004.-We developed transgenic mice with targeted expression of human renin (hREN) and human angiotensinogen (hAGT) to either neurons (N-AII mice) or glia (G-AII mice) to test the hypothesis that neuronal and glial ANG II may have differential function. Since baseline blood pressure (BP) did not differ between the models (109 Ϯ 3 vs. 114 Ϯ 4 mmHg), we stressed the BP regulatory pathway by measuring the heart rate (HR) (baroreflex) response to phenylephrine-and nitroprusside-induced changes in arterial BP. The midpoint of the baroreflex curve (BP50) was reset to a significantly higher BP in N-AII mice (131 Ϯ 5 mmHg) compared with littermate controls (115 Ϯ 3 mmHg). Baroreflex gain (slope of BP-HR relation) was similar in N-AII and control mice (12 Ϯ 1 vs. 14 Ϯ 2 beats⅐min Ϫ1 ⅐mmHg Ϫ1 ). In contrast, G-AII mice exhibited less of an increase in BP50 (125 Ϯ 5 mmHg) but a larger decrease in baroreflex gain (8 Ϯ 1 beats⅐min Ϫ1 ⅐mmHg Ϫ1 ) compared with both control and N-AII mice. Differences in BP50 and gain between N-AII, G-AII, and control mice persisted after parasympathetic blockade with atropine but were eliminated after sympathetic blockade with propranolol, indicating the effects of ANG II were selective for cardiosympathetic arm of the reflex. ANG II-like immunoreactivity was observed more prominently around the paraventricular nucleus and nucleus tractus solitarii in G-AII mice but more prominently in the ventrolateral medulla in N-AII mice. We conclude that ANG II differentially modulates baroreflex control of HR in mice producing ANG II in neurons vs. glia, and its differential function may reflect regional differences in the production of ANG II in cardiovascular control nuclei of the brain. renin-angiotensin system; brain; transgenic animal; sympathetic nervous system THE ARTERIAL BAROREFLEX is a major regulator of arterial pressure (AP) and cardiovascular function and acts to buffer changes in AP in part by changing heart rate (HR). The baroreflex has been studied extensively in animal models and humans. Clinical studies have demonstrated that hypertension is accompanied by a modulation of baroreflex function (3,4,11,23,32); and it is known that this modulation occurs by one of two mechanisms. In the first, the baroreflex curve is shifted or reset to a higher pressure, whereas in the second there is a decreased sensitivity of the reflex as measured by a decreased slope (or attenuated gain) of the baroreflex curve. These mechanisms have been documented in many experimental animal models of hypertension (10,17,25,26).There is considerable evidence that circulating ANG II plays a critical role in the baroreflex control of HR by modulating either the set point or sensitivity of the reflex (7,24,25,34). For example, chronic intracerebroventricular (ICV) infusion of ANG II decreased baroreflex gain and bloc...

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A Mathematical Model to Assess Changes in the Baroreceptor Reflex

Cited by 371 publications

References 17 publications

Central Ghrelin Modulates Sympathetic Activity in Conscious Rabbits

Central Ghrelin Modulates Sympathetic Activity in Conscious Rabbits

Difference between Halothane and Barbiturate Anesthesia in the Influence of Cerebral Ischemia on the Vagal Baroreflex in Dogs.

Differential modulation of baroreflex control of heart rate by neuron- vs. glia-derived angiotensin II

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