Blood pressure control by the renin-angiotensin system in normotensive subjects. Assessment by angiotensin converting enzyme and renin inhibition.

Kiowski, Wolfgang; Linder, Lilly; Kleinbloesem, Cornelis H.; Brummelen, P. Van; Bühler, Fritz R.

doi:10.1161/01.cir.85.1.1

Cited by 95 publications

(16 citation statements)

References 55 publications

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“…Although it is not universally accepted, ACE inhibitors do cause a small fall in blood pressure in salt replete volunteers (Kiowski et al, 1992). In this present study, there were considerable reductions in blood pressure despite a low dose of enalapril.…”

Section: Discussionsupporting

confidence: 40%

Haemodynamic and hormonal responses to oral enalapril in salt depleted normotensive man.

Elliott

Modesti

et al. 1993

Brit J Clinical Pharma

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A combination of dietary sodium restriction (40 mmol day‐1) and frusemide pretreatment has been used to activate the renin angiotensin system (RAS) in order to characterise the haemodynamic and hormonal responses to enalapril in young normotensives. Enalapril significantly reduced supine blood pressure with a mean maximum fall of 19 +/‐ 7.6, compared with 6.5 +/‐ 6.8 mm Hg with placebo. Similar but greater responses were seen in erect blood pressure. Mean maximal plasma ACE inhibition (78 +/‐ 5.7%) was associated with a significant increase in PRA from 5.2 +/‐ 2.1 ngAI ml‐1 h‐1 to a peak of 29.1 +/‐ 6 ngAI ml‐1 h‐ 1. This simple well tolerated regimen produced consistent RAS activation and gave readily measurable falls in blood pressure following enalapril. This model may be used to undertake detailed assessments of ACE inhibition, renin inhibition and angiotensin receptor blockade.

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Section: Discussionsupporting

confidence: 40%

Haemodynamic and hormonal responses to oral enalapril in salt depleted normotensive man.

Elliott

Modesti

et al. 1993

Brit J Clinical Pharma

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“…3,4 Briefly, forearm blood flow was measured by strain-gauge plethysmography after intra-arterial infusion of increasing doses of the endothelium-dependent vasodilators bradykinin (infusion rates: 100, 200, and 400 ng/min) and acetylcholine (infusion rates: 7.5, 15, and 30 g/min) 16,17 and of the endothelium-independent vasodilator sodium nitroprusside (infusion rates: 0.8, 1.6, and 3.2 g/min). 18 Drugs sequence was randomized to avoid bias related to the order of infusion.…”

Section: Endothelial Function Studiesmentioning

confidence: 99%

Peroxisome Proliferator–Activated Receptor-γ Activation With Pioglitazone Improves Endothelium-Dependent Dilation in Nondiabetic Patients With Major Cardiovascular Risk Factors

2006

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“…Recent inhibitor, thus indicating a role of NO in the late phase of studies strongly indicate that kinin participates in the control bradykinin-induced hypotension (Rees et al, 1990). However, of blood pressure (BP) (Kiowski et al, 1992; Cachofeiro et similar results were not obtained by O'Shaughnessy et al al., 1992;Pellacani et al, 1992). It has been suggested that (1992), thus questioning the role of NO as a mediator in the hypotensive effect of bradykinin is mediated through the bradykinin-induced hypotension.…”

Section: Introductionmentioning

confidence: 96%

The role of nitric oxide, adrenergic activation and kinin‐degradation in blood pressure homeostasis following an acute kinin‐induced hypotension

Bjørnstad-Østensen

Berg

1994

British J Pharmacology

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1 Nitric oxide (NO) has been suggested as the mediator of the vascular response to bradykinin. In the present study, we found that NO did not mediate the hypotensive response to bradykinin. In addition, the significance of kininase II in terminating a kinin-induced hypotension and the role of the adrenergic system in compensating for the acute fall in blood pressure (BP) was established. 2 In normal rats, the NO-synthase inhibitor Nw-nitro-L-arginine methyl ester (L-NAME) induced a rise in basal BP (ABP =40±6 mmHg, P<0.0014) which was not altered by pretreatment with phentolamine (ABP = 50 ± 6 mmHg, NS). L-NAME did not attenuate the acute fall in BP in response to bradykinin (3-30 1gkg-') or kallikrein (6-300 1gkg-'). However, a significant decrease was observed in the duration of the hypotensive response (P<0.027). This shorter duration was not observed after pretreatment with phentolamine in addition to L-NAME. Phentolamine alone prolonged the hypotensive response to bradykinin (P<0.04). These experiments confirm the role of NO-formation as a hypotensive component in BP homeostasis but not the role of NO as a mediator in kinin-induced hypotension. It further shows that the continuous NO-release also impedes the compensatory adrenergic hypertensive response following the acute fall in BP induced by bradykinin. 3 The hypertensive respose to intravenously administered phenylephrine was found to be unchanged by preadministration of L-NAME (NS) thus showing that L-NAME did not change the sensitivity to the adrenergic response. In a separate protocol on L-NAME-treated rats we found no difference in heart rate (NS) during the recovery period following bradykinin before as compared to after administration of phentolamine. It was therefore concluded that the observed alterations in the duration of the hypotensive response were most probably due to changes in peripheral vascular resistance. 4 To confirm further that NO is not a mediator in kinin-induced hypotension, we used an experimental model where the response to bradykinin was profonged by preventing kinin degradation by kininase II-converting enzyme inhibitor (CEI). To produce a hypotensive response purely dependent on kinin, the studies were performed after removal of the renin-angiotensin system by nephrectomy (Nx). In this model, bradykinin (6 pg kg-', i.v.) induced a prolonged hypotensive response. Pretreatment with L-NAME did not alter the magnitude or the progression of the hypotensive response to bradykinin, thus confirming that NO was not a mediator in BK-induced hypotension. 5 To study the mechanisms involved in terminating the hypotensive response to bradykinin, the results from the Nx CEI-treated rats were compared with Nx animals not treated with CEL. In the latter group, bradykinin induced a short hypotensive response, i.e. 0.5 ± 0.1 min as compared to the 17 ± 1 min after CEI (P<0.003). After kininase II-inhibition (and L-NAME), BP recovery was totally dependent on the adrenergic system, since phentolamine prevented a recovery in BP during the exper...

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Blood pressure control by the renin-angiotensin system in normotensive subjects. Assessment by angiotensin converting enzyme and renin inhibition.

Cited by 95 publications

References 55 publications

Haemodynamic and hormonal responses to oral enalapril in salt depleted normotensive man.

Haemodynamic and hormonal responses to oral enalapril in salt depleted normotensive man.

Peroxisome Proliferator–Activated Receptor-γ Activation With Pioglitazone Improves Endothelium-Dependent Dilation in Nondiabetic Patients With Major Cardiovascular Risk Factors

The role of nitric oxide, adrenergic activation and kinin‐degradation in blood pressure homeostasis following an acute kinin‐induced hypotension

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