Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity

Guo, G. B.; Abboud, François M.

doi:10.1152/ajpheart.1984.246.1.h80

Cited by 125 publications

(123 citation statements)

References 0 publications

Supporting

Mentioning

106

Contrasting

Order By: Relevance

“…It is known the attenuating effect of angiotensin II on baroreflex sensitivity. 24 Moreira et al 25 have reported the existence of a close relationship between overactivity of renin-angiotensin system and the impairment of baroreflex control of heart rate in rats with renal hypertension. Reduction in baroreflex sensitivity present in the acute phase of 2K 1C hypertension in rats is mediated, at least in part, by renin-angiotensin system activation.…”

Section: Discussionmentioning

confidence: 99%

Mild chronic renal insufficiency induces sympathetic overactivity

Tinucci

et al. 2001

J Hum Hypertens

View full text Add to dashboard Cite

The objectives of this study were to evaluate baseline sympathetic nerve activity as well as the mechanisms of sympathetic overactivity in mild chronic renal insufficiency hypertension. Seven hypertensives with mild renal insufficiency, seven hypertensives with normal renal function and seven normotensives, age and weight-matched were studied on one session to evaluate baseline muscle sympathetic nerve activity measured in the peroneal nerve. The mild renal insufficiency hypertensives and the hypertensives with normal renal function were also studied to evaluate arterial baroreflex control of muscle sympathetic nerve activity assessed by increasing and decreasing blood pressure through continuous infusion of phenylephrine and sodium nitroprusside respectively. Baseline muscle sympathetic nerve activity was significantly higher in mild renal insufficiency hypertensives (34 bursts/min) when com-

show abstract

Section: Discussionmentioning

confidence: 99%

Mild chronic renal insufficiency induces sympathetic overactivity

Tinucci

et al. 2001

J Hum Hypertens

View full text Add to dashboard Cite

show abstract

“…Many investigators have observed that ANG II decreases baroreflex sensitivity while blockade of the renin-angiotensin system increases it (7,9,12,19,34). Others have observed resetting with no change in sensitivity (9,13,24,30).…”

Section: Discussionmentioning

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

View full text Add to dashboard Cite

. 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...

show abstract

“…These data suggest that ACE inhibitors, more than antirenin immunization, reduce the generation of angiotensin II within the central nervous system, where it specifically depresses cardiac baroreceptor reflex responses to increases, but not to decreases, in blood pressure. 27 - 28 However, it has been recently shown that brain ACE was not consistently decreased by most of the ACE inhibitors. 29 In addition, antirenin immunization also tended to increase the baroreceptor reflex sensitivity.…”

Section: Figure 4 Bar Graphs Showing the Free Urinary Catecholaminesmentioning

confidence: 99%

Antirenin immunization versus angiotensin converting enzyme inhibition in rats.

Julien

Michel

et al. 1990

Hypertension

View full text Add to dashboard Cite

The effects of specific active immunization against renin were compared with those of chronic angiotensin converting enzyme (ACE) inhibition. Male spontaneously hypertensive rats (SHR) were immunized (SHR-I) (n=10) against pure murine renin (four injections of 30 /ig/kg s.c) or received (SHR-P) (n=ll) a converting enzyme inhibitor (perindopril, 2 mg/kg/day per os for 4 weeks). Sham-immunized SHR (SHR-S) (n=12) and normotensive Wistar-Kyoto (WKY-S) (n=12) rats served as controls. At 15 weeks of age, 24-hour average blood pressure was obtained in freely moving rats using intra-aortic pressure recording with computer analysis. Antirenin immunization induced high circulating titers of antibodies, a fall in plasma renin activity (-95%), and urinary excretion of mineralocorticoids. Perindopril abolished the pressor response to angiotensin I, whereas plasma ACE was only partly (-56%) decreased. It also increased plasma renin activity and did not alter the urinary excretion of steroids. Both immunization and perindopril allowed the blood pressure of SHR to return to the level of WKY-S rats and reduced the left ventricular weight These decreases were associated with an elevated sympathetic nervous system activity as indicated by increases in the urinary excretion of catecholamines and their metabolites. It is concluded that, apart from an unaltered steroid synthesis, most of the cardiovascular effects of chronic ACE inhibition are similar to those of antirenin immunization, thus indicating that blockade of the circulating and renal reninangiotensin system accounts for most of the effects of ACE inhibitors. (Hypertension 1990; 16:80-88)

show abstract

Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity

Cited by 125 publications

References 0 publications

Mild chronic renal insufficiency induces sympathetic overactivity

Mild chronic renal insufficiency induces sympathetic overactivity

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

Antirenin immunization versus angiotensin converting enzyme inhibition in rats.

Contact Info

Product

Resources

About