Hypotensive effect of captopril. Role of bradykinin and prostaglandinlike substances.

Pontieri, Vera; Lopes, Oswaldo Ubrı́aco; Ferreira, S. H.

doi:10.1161/01.hyp.15.2_suppl.i55

Cited by 20 publications

(12 citation statements)

References 12 publications

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“…Therefore, these results suggest that this inhibitory effect is dependent on potentiation of the hypotensive effect of bradykinin. These data are in accordance with previous findings describing the effect of bradykinin antagonism on the hypotensive and anti-hypertensive actions of kininase II inhibitors (18)(19)(20). Potentiation of the bradykinin effects by captopril (5) may be a mechanism that, by interacting with the inhibition of angiotensin II formation, may explain part of the inhibitory effect of captopril observed in the present study.…”

Section: Intravenous Effect Of Bradykinin Before and After Hoe 140 (Psupporting

confidence: 94%

Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats

Moura

Leão

1997

Braz J Med Biol Res

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The aim of the present study was to investigate the role of bradykinin in the inhibitory action of captopril in hypertension induced by L-NAME in anesthetized rats. Male Wistar rats (260-320 g) were anesthetized with chloralose and arterial blood pressure was recorded with a polygraph pressure transducer. The hypertensive effect of L-NAME was studied in rats pretreated with saline, captopril or HOE 140 plus captopril. The effect of captopril was also studied during the sustained pressor effect of L-NAME. The acute pressor effect of L-NAME (10 mg/kg, iv) was significantly reduced by iv pretreatment with 2 mg/kg captopril (∆ increase of 49 ± 4.9 mmHg reduced to 20 ± 5.4 mmHg, P = 0.01). The pressor effect of L-NAME (∆ increase of 38 ± 4.8 mmHg) observed in rats pretreated with captopril and HOE 140 (0.1 mg/kg, iv) was not significantly different from that induced by L-NAME in rats pretreated with saline (P = 0.09). During the sustained pressor effect induced by L-NAME (∆ increase of 49 ± 4.9 mmHg) captopril induced a significant (P<0.05) reduction in arterial blood pressure (∆ decrease of 22 ± 3.0 mmHg). The present results demonstrate that the acute pressor effect of L-NAME is reduced by captopril and this inhibitory effect may be partly dependent on the potentiation of the vasodilator actions of bradykinin.

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Section: Intravenous Effect Of Bradykinin Before and After Hoe 140 (Psupporting

confidence: 94%

Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats

Moura

Leão

1997

Braz J Med Biol Res

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“…Finally, in addition to their ability to inhibit conversion of angiotensin I to angiotensin II, ACE inhibitors also inhibit inactivation of bradykinins. 18 Thus, we cannot rule out the possibility that cilazapril 10 and perindopril 11 attenuated cerebral arteriolar remodeling in SHRSP by increasing availability of bradykinins rather than decreasing availability of angiotensin II.…”

Section: Baumbach Et Al Vascular Structure In Renin-angiotensinogen Mmentioning

confidence: 96%

Cerebral Arteriolar Structure in Mice Overexpressing Human Renin and Angiotensinogen

2003

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Abstract-We examined the hypothesis that the renin-angiotensin system plays an important role in vascular remodeling (defined as reduced external diameter) during chronic hypertension. We measured pressure, diameter, and crosssectional area of the vessel wall in maximally dilated cerebral arterioles in transgenic mice that overexpress both human renin and human angiotensinogen and in spontaneously hypertensive mice, a model of chronic hypertension that is thought to develop independently of the renin-angiotensin system. . During maximal dilatation, the stress-strain curves in cerebral arterioles of transgenically hypertensive mice and spontaneously hypertensive mice were shifted to the right of the curves in corresponding controls, an indication that arteriolar distensibility was increased in the transgenically and spontaneously hypertensive groups. Thus, cerebral arterioles undergo remodeling and hypertrophy in transgenically hypertensive mice, but only hypertrophy in spontaneously hypertensive mice. These findings support the hypothesis that the renin-angiotensin system is an important determinant of vascular remodeling during chronic hypertension. Key Words: renin-angiotensin system Ⅲ mice Ⅲ vasculature Ⅲ remodeling Ⅲ hypertrophy Ⅲ hypertension, chronic C hronic hypertension alters the structure and mechanics of cerebral arterioles. Cerebral arterioles in spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) undergo both hypertrophy of the vessel wall and reduction in external diameter (remodeling). 1,2 Despite hypertrophy, cerebral arterioles undergo a paradoxical increase in passive distensibility of the vessel wall during chronic hypertension in SHRSP. 3 Because these alterations may contribute to the increased risk of stroke that accompanies chronic hypertension, it is important to examine determinants of these alterations in the cerebral circulation, as opposed to other vascular beds, so that we may better understand the link between chronic hypertension and stroke.Alterations in vascular structure during chronic hypertension may result from a number of determinants, including arterial pressure, 4 neurohumoral factors, 5,6 and endotheliumderived factors. 7-9 A determinant of particular interest with respect to vascular remodeling has been the renin-angiotensin system. This interest was stimulated by previous studies in which we found that angiotensin-converting enzyme (ACE) inhibitors, but not hydralazine or propranolol, attenuate remodeling of cerebral arterioles in SHRSP. 10,11 Because the ACE inhibitors lowered arterial pressure in SHRSP more effectively than hydralazine and propranolol, however, we were unable to draw definitive conclusions from these studies with regard to the direct effects of the ACE inhibitor on cerebral vascular remodeling and hypertrophy, as opposed to the effects of arterial pressure per se.A major goal of this study was to examine further the hypothesis that the renin-angiotensin system plays an important role in vascular remodeling during chronic hypertension. T...

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“…In addition to their ability to inhibit conversion of angiotensin I to Ang II, ACE inhibitors also inhibit inactivation of bradykinins. 16 It cannot be ruled out, therefore, that perindopril may have attenuated cerebral arteriolar remodeling in SHRSP by increasing availability of bradykinins rather than decreasing availability of Ang II.…”

Section: Remodelingmentioning

confidence: 99%

Effects of an Angiotensin-Converting Enzyme Inhibitor and a β-Blocker on Cerebral Arterioles in Rats

Chillon

Baumbach

1999

Hypertension

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Abstract-We examined the effects of an angiotensin-converting enzyme inhibitor, perindopril, and a ␤-blocker, propranolol, on cerebral arterioles in stroke-prone spontaneously hypertensive rats (SHRSP). The structure and mechanics of cerebral arterioles were examined in untreated Wistar-Kyoto rats (WKY) and SHRSP that were untreated or treated for 3 months with a high (2 mg/kg per day) or a low (0.3 mg/kg per day) dose of perindopril or propranolol (250 mg/kg per day) alone or in combination with the low dose of perindopril. We measured pressure, external diameter, and cross-sectional area of the vessel wall (CSA) in maximally dilated (with EDTA) cerebral arterioles. In contrast, treatment of SHRSP with the low dose of perindopril or propranolol alone did not normalize arteriolar pulse pressure (24Ϯ1 and 21Ϯ1 mm Hg) and failed to prevent increases in CSA (1282Ϯ77 and 1267Ϯ94 m 2 ). Treatment with either dose of perindopril or the combination of propranolol and perindopril significantly increased external diameter in cerebral arterioles of SHRSP (99Ϯ3, 103Ϯ2, and 98Ϯ3 m vs 87Ϯ2 m in untreated SHRSP; PϽ0.05), whereas propranolol alone did not (94Ϯ3 m; PϾ0.05). These findings suggest that effects of angiotensin-converting enzyme inhibitors on cerebral arteriolar hypertrophy in SHRSP may depend primarily on their effects on arterial pressure, particularly pulse pressure, whereas their effects on cerebral arteriolar remodeling (defined as a reduction in external diameter) may be pressure independent. (Hypertension. 1999;33:856-861.)

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Hypotensive effect of captopril. Role of bradykinin and prostaglandinlike substances.

Cited by 20 publications

References 12 publications

Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats

Participation of kinins in the inhibitory action of captopril on acute hypertension induced by L-NAME in anesthetized rats

Cerebral Arteriolar Structure in Mice Overexpressing Human Renin and Angiotensinogen

Effects of an Angiotensin-Converting Enzyme Inhibitor and a β-Blocker on Cerebral Arterioles in Rats

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