Angiotensin-converting enzyme inhibitor resets baroreceptor reflexes in conscious dogs.

Hatton, R; Clough, D.P.; Faulkner, Kimberly A.; Conway, James

doi:10.1161/01.hyp.3.6.676

Cited by 57 publications

(37 citation statements)

References 33 publications

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“…But the mechanism of the decline in arterial pressure in response to ACE inhibitor in immature lambs of the current study is not known. Studies in adult animals suggest that A11 is involved in the maintenance of arterial pressure during sodium depletion through involvement in homeostatic baroreceptor reflex activity as well as direct vasoconstrictor action (7). The present study demonstrated a decline in arterial pressure in response to ACE inhibitor in immature lambs, which was not accompanied by an increase in TBF (ml/min.g) TBF (ml/m~n.g) heart rate.…”

Section: Resultssupporting

confidence: 40%

Organ Tissue Blood Flow Responses to Hypoxemia in Lambs: Effect of Angiotensin Converting Enzyme Inhibitor

et al. 1983

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SummaryChronically-catheterized lambs (n = 21), 2-38 days of age, were studied to test the hypothesis that the products of angiotensin converting enzyme (ACE) activity are involved in control of baseline arterial pressure and organ tissue blood flow and the redistribution of organ tissue blood flow in response to normocapnic hypoxemia in the maturing lamb. ACE activity was inhibited by administration of captopril 12.5 pg/(kg*min)], which significantly ( P < 0.01) decreased arterial concentrations (mean + S.D.) of angiotensin-I1 (from 105.0 + 33.9 to 67.0 + 25.9 pg/ml) and aldosterone (from 115.0 + 105.0 to 53.8 + 28.6 pg/ml) and inhibited by greater than 90% the vasopressor response to an intravenous bolus of angiotensin-I (1 pg/kg). Baseline mean arterial pressure was significantly ( P < 0.01) decreased from 78 + 8 to 66 + 10 mmHg) and remained depressed during hypoxemia (67 + 12 mmHg) and recovery (62 + 9 mmHg) periods. Baseline heart rate was unchanged by ACE inhibition (from 181 + 33 to 188 + 35 beats/min) but increased ( P < 0.01) significantly in response to hypoxemia (to 233 + 52 beats/min). Baseline heart, adrenal, jejunum, ileum, and skeletal muscle tissue blood flow, measured by radiolabeled microspheres, were not significantly (P > 0.05) changed by ACE inhibitor. Baseline liver tissue blood flow increased slightly [from 0.10 + 0.10 to 0.16 + 0.12 ml/(min*g)] but significantly ( P < 0.05) during ACE inhibitor treatment, and spleen tissue blood flow decreased significantly [from 2.54 + 1.03 to 1.31 + 0.61 ml/(min*g)]. Normocapnic hypoxemia (Poz 42 + 6 torr; oxyhemoglobin saturation 50.7 + 18.0%) for 30 min during ACE inhibition was associated with increased ( P < 0.01) heart [from 2.72 + 1.52 to 8.87 + 5.78 ml/(min*g)] and adrenal [from 2.75 + 1.88 to 6.43 + 2.82 ml/(min*g)l tissue blood flow, decreased (P < 0.01) spleen [from 1. 2.00 ml/(min*g)] demonstrated a greater fall in blood flow to these tissues in response to hypoxemia in control lambs. Thus, the products of ACE may be important in maintenance of baseline arterial pressure in the maturing animal. Furthermore, these products may be important in splanchnic vasoconstrictive responses to stress such as hypoxemia in the maturing animal. Abbreviations AI, angiotensin I AII, angiotensin I1 ACE, angiotensin converting enzyme Aldo, aldosterone HR, heart rate MAP, mean arterial pressure RAA, renin-angiotensin-aldosterone Activity of the renin-angiotensin-aldosterone (RAA) system is increased in newborns in comparison to adults (12, 15, 18-20, 24, 25), and decreases rapidly with increasing postnatal age (6,10,23,25,27,29). Responsiveness of this system may also vary with postnatal age (29). The contribution of this system to the control of organ tissue blood flow in newborn animals is unknown. Furthermore, its importance in pathophysiologic conditions, such as hypoxemia, during maturation is not clear. Activity of RAA system is increased in response to hypoxemia (1,14,22,30,32) and is accompanied by a redistribution of organ tissue arterial blood flow (...

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Section: Resultssupporting

confidence: 40%

Organ Tissue Blood Flow Responses to Hypoxemia in Lambs: Effect of Angiotensin Converting Enzyme Inhibitor

et al. 1983

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“…Others have observed resetting with no change in sensitivity (9,13,24,30). These two mechanisms have different physiological and pathophysiological implications since baroreflex resetting preserves shortterm buffering of acute BP changes, whereas reduced baroreflex sensitivity impairs short-term buffering of acute BP changes.…”

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

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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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“…In conscious, sodium-depleted dogs, captopril elicited a resetting of the whole baroreceptor reflex, and it was suggested that, besides having a central effect, the converting enzyme inhibitor might be acting peripherally at the receptor level. 8 Captopril can affect baroreceptor activity directly by an intrinsic effect, by reducing the circulatory levels of angiotensin II, or by both. It was previously demonstrated in experiments with single fibers that angiotensin II increases the firing rate of the carotid sinus nerve of the cat, but the response is abolished by reserpine.…”

Section: Discussionmentioning

confidence: 99%

Antihypertensive drugs distinctly modulate the rapid resetting of the baroreceptors.

Abreu

Salgado

1990

Hypertension

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We investigated the distinct ability of various antihypertensive drugs to modulate the extent (%) of rapid (15 minutes) resetting of the baroreceptors of normotensive rats to hypertensive levels. In one protocol, hemorrhage produced a complete resetting to hypotension in rats chronically treated (6 days) with captopril. Also, hemorrhage produced only partial resetting in rats acutely treated (10-15 minutes before baroreceptor recording) with captopril and in control (untreated) rats (73±7% and 49±5%, respectively). In another protocol, all vasodilators produced hypotension in normotensive rats. Nifedipine produced complete (93 ±4%) resetting to hypotension, whereas prazosin produced near-maximal (83 ±3%) resetting. The remaining drugs studied (phenoxybenzamine, trimethaphan, and MgSO 4 ) induced a partial resetting (63 ±7%, 63 ±9%, and 50 ±5%, respectively) that did not differ significantly from the extent observed with hemorrhage in control (untreated) rats. These results demonstrate that different antihypertensive drugs distinctly modulate rapid baroreceptor resetting to hypotensive levels and that nifedipine and long-term treatment with captopril associated with hemorrhage modulate rapid resetting to hypotension in a more efficient manner. (Hypertension 1990;15(suppl I):I-63-I-67)

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Angiotensin-converting enzyme inhibitor resets baroreceptor reflexes in conscious dogs.

Cited by 57 publications

References 33 publications

Organ Tissue Blood Flow Responses to Hypoxemia in Lambs: Effect of Angiotensin Converting Enzyme Inhibitor

Organ Tissue Blood Flow Responses to Hypoxemia in Lambs: Effect of Angiotensin Converting Enzyme Inhibitor

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

Antihypertensive drugs distinctly modulate the rapid resetting of the baroreceptors.

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