Antihypertensive drugs distinctly modulate the rapid resetting of the baroreceptors.

Abreu, Gabriel; Salgado, Hélio César

doi:10.1161/01.hyp.15.2_suppl.i63

Cited by 10 publications

(7 citation statements)

References 10 publications

(12 reference statements)

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“…Normotensive rats treated acutely with captopril, enalapril, or DuP 753 presented a slight but significant fall in MAP associated with a partial leftward curve shift and partial threshold shift to hypotensive levels. These data confirm previous observations from our laboratory, 7 based on changes of systolic pressure threshold for baroreceptor activation, that acute ACE inhibition with captopril facilitates rapid resetting to hypotensive levels. Nevertheless, the present study also demonstrates that acute ACE inhibition or blockade of Ang II receptors increases baroreceptor sensitivity.…”

Section: Discussionsupporting

confidence: 91%

“…5 Various antihypertensive drugs modulate rapid baroreceptor resetting to hypotensive levels, and among these, long-term (7-day) blockade of angiotensin II (Ang II) generation with captopril most efficiently modulates rapid resetting. 6 - 7 Vasoactive peptides such as Ang II also affect baroreceptor function. 8 - 10 Experiments in vitro in an aortic arch preparation 8 have demonstrated that as Ang II concentration increases, the pressurenerve activity curves shift in a parallel manner to higher pressures, requiring a substantially higher pressure threshold for baroreceptor activation.…”

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confidence: 99%

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Chronic converting enzyme inhibition facilitates baroreceptor resetting to hypertensive levels.

Silva

Silva²,

Salgado³

et al. 1994

Hypertension

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We investigated the acute and chronic effects of converting enzyme inhibitors (captopril or enalapril) and of angiotensin II receptor blockade (DuP 753) on rapid (30-minute) baroreceptor resetting elicited by a prompt and sustained hypertensive response provoked by aortic constriction. Pressure-nerve activity curves, pressure at 50% of maximal baroreceptor activity, baroreceptor gain (slope of the curve), and systolic threshold pressure for baroreceptor activation were determined as indexes of baroreceptor function. A slight fall in mean arterial pressure after acute treatment with the converting enzyme inhibitor or DuP 753 was accompanied by a partial leftward curve shift, which is associated with a partial threshold shift and increase in gain. A maintained hypertensive stimulus caused a partial rightward curve shift and partial (49% to 56%) threshold shift to hypertensive levels in both acutely treated and control rats. The hypertensive stimulus provoked a partial rightward curve shift and complete (88% to 94%) threshold shift to hypertensive levels in chronically treated rats. 8 have demonstrated that as Ang II concentration increases, the pressurenerve activity curves shift in a parallel manner to higher pressures, requiring a substantially higher pressure threshold for baroreceptor activation. Accordingly, endogenous vasoactive peptides such as Ang II might also modulate rapid resetting. Changes in pressure threshold are linearly related to changes in conditioning pressure over a wide range, 11 and rapid resetting is usually recognized as partial because the magnitude of the shift in pressure threshold is approximately 50% or less 61113 of the magnitude of change in conditioning pressure. Nevertheless, when rapid resetting was driven to hypotensive levels with the conditioning pressure under the influence of an antihypertensive agent, the baroreceptors totally adapted within 15 minutes. Correspondence to Dr H61io C. Salgado, Department of Physiology, School of Medicine, USP, 14049-900 Ribeirao Preto, SP, Brazil.To our knowledge the effect of ACE inhibition on rapid baroreceptor resetting has not yet been investigated in any hypertensive model. Therefore, we evaluated in the present study the extent of rapid (30-minute) resetting elicited by a prompt and sustained rise in arterial pressure in nonnotensive rats treated acutely (15 minutes) or chronically (7 days) with ACE inhibitors, captopril or enalapril, and an ATi receptor antagonist, DuP 753. We also investigated the role played by bradykinin potentiation on rapid baroreceptor resetting during blockade of ACE. 14 MethodsExperiments were performed on anesthetized (thiopental sodium, 40 mg/kg IP) normotensive male Wistar rats (250 to 300 g) in accordance with the guiding principles of the American Physiological Society. Catheters were placed into the right common carotid artery for measurement of arterial pressure, the right femoral artery for withdrawal and reinfusion of blood, and the right femoral vein for the administration of drugs. A pneuma...

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 99%

Chronic converting enzyme inhibition facilitates baroreceptor resetting to hypertensive levels.

Silva

Silva²,

Salgado³

et al. 1994

Hypertension

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“…5 -7 On the other hand, recent investigations have demonstrated that various antihypertensive drugs including calcium antagonists and angiotensin-converting enzyme (ACE) inhibitors, which have become widely used in clinical practice, differently modulate acute resetting of the baroreceptors to hypotension. 8 - 9 We inferred, therefore, that various produced a leftward shift of the arterial pressure-aortic nerve activity relation to a similar extent (threshold pressure, 77±1 mm Hg, P<.Q5) in spontaneously hypertensive rats. In addition, treatment with the four agents equally augmented the maximum gain in spontaneously hypertensive rats (2.13±0.09% maximum/mm Hg, P<.05).…”

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confidence: 69%

“…elicited acute baroreceptor resetting. On the other hand, de Abreu and Salgado 9 reported that acute baroreceptor resetting induced by another calcium antagonist, nifedipine, was greater than that induced by hemorrhage. In vitro studies have also revealed conflicting results, suggesting that baroreceptor activity was affected 24 or not affected 25 by calcium antagonists.…”

Section: Discussionmentioning

confidence: 97%

“…Regarding ACE inhibitors, it has been reported that captopril facilitated acute baroreceptor resetting to hypotension. 9 Based on these studies, the hypothesis was put forward that chronic antihypertensive treatment with various types of agents could exert different effects on the baroreceptor function. To examine this hypothesis, we administered one of four agents (a diuretic, a /3-adrenergic blocker, a calcium channel blocker, and an ACE inhibitor) to relatively young SHRs (10 weeks of age) for 2 weeks.…”

Section: Discussionmentioning

confidence: 99%

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Effects of antihypertensive agents on baroreceptor function in early hypertensive rats.

et al. 1994

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To investigate the effects of antihypertensive treatment with four currently used agents (trichlormethiazide, atenolol, nicardipine, and enalapril) on the arterial baroreceptor function at the early phase of hypertension, we administered the agents to spontaneously hypertensive rats and WistarKyoto rats from 8 to 10 weeks of age and examined the aortic nerve activity function. In untreated spontaneously hypertensive rats, the relation between the arterial pressure and aortic nerve activity was shifted to the right, that is, to a higher pressure level (threshold pressure, 90±3 versus 76±1 mm Hg, P<.05), and the maximum gain which was obtained by logistic function analysis was depressed (1.55±0.08% versus 2.18±0.13% maximum/mm Hg, f<.01) as compared with untreated Wistar-Kyoto rats. An equivalent decrease in arterial pressure with each of the four agents (-20±l mm Hg, P<.01) B aroreceptor activity transmitted to the central nervous system (CNS) is a primary signal concerning moment-to-moment alterations in arterial pressure and represents a fundamental mechanism in the neural control of the circulation because it triggers reflex inhibition of sympathetic nerve activity and excitation of parasympathetic nerve activity that buffers the rise in pressure. It is known that the baroreceptor function is depressed in several forms of hypertension. 1 " 3 Impaired baroreceptor input to the CNS elicits instability of the circulation, 4 which tends in turn to lead to increases in cardiovascular morbidity and mortality. Agents that effectively potentiate the baroreceptor function are considered preferable in the treatment of hypertension. Early studies have shown that conventional antihypertensive therapy with combinations of drugs (diuretics, vasodilators, and adrenergic antagonists) increased the baroreceptor sensitivity in spontaneously hypertensive rats (SHRs). classes of antihypertensive agents might exert distinct effects on the baroreceptor function through specific pharmacological actions when administered chronically to hypertensive subjects. To test this hypothesis, we treated SHRs with one of four currently used agents (a diuretic, a j3-adrenergic blocker, a calcium channel blocker, and an ACE inhibitor) for 2 weeks and examined the effects on the aortic baroreceptor function. Moreover, we used relatively young SHRs (10 weeks of age) in which the characteristics of the aorta are less damaged by hypertension 3

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Cardiovascular Analysis In Vivo

Gralinski¹,

Neves²,

Tiniakova³

2016

Drug Discovery and Evaluation: Pharmacological Assays

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Antihypertensive drugs distinctly modulate the rapid resetting of the baroreceptors.

Cited by 10 publications

References 10 publications

Chronic converting enzyme inhibition facilitates baroreceptor resetting to hypertensive levels.

Chronic converting enzyme inhibition facilitates baroreceptor resetting to hypertensive levels.

Effects of antihypertensive agents on baroreceptor function in early hypertensive rats.

Cardiovascular Analysis In Vivo

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