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Cardiovascular Research 1998 38(1):215-220; doi:10.1016/S0008-6363(97)00288-5
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Dissociation between the renal effects of angiotensin I and II in sodium-restricted normal subjects

Marielle M.E Krekels, Wilko Spiering, Nicolaas C Schaper, Alphons J.H.M Houben and Peter W de Leeuw*

Department of Internal Medicine/Cardiovascular Research Institute, University Hospital, Maastricht, Netherlands

* Corresponding author: Tel.: +31 (43) 387-7005; Fax: +31 (43) 387-5006.

Objective: To determine whether the effects of angiotensin I (AngI) in humans can be explained entirely by its plasmatic conversion to angiotensin II (AngII). Methods: Ten healthy male volunteers on a sodium-restricted diet were studied on two separate occasions, during which, in random order, AngI or AngII was infused in increasing doses of 0.3, 1 and 3 pmol·kg–1·min–1. Mean arterial pressure (MAP), effective renal plasma flow (ERPF), glomerular filtration rate (GFR), active plasma renin concentration (APRC), AngII, aldosterone (Aldo) and catecholamines were assessed at baseline, after each dose of AngI or AngII and 30 and 60 min after discontinuation of the AngI/AngII infusion. Results: The rise in plasma AngII was significantly less during AngI infusion as compared to AngII infusion (P<0.05). Changes in MAP, Aldo and GFR, however, were comparable during both infusions. In the kidney, on the other hand, the decrements in APRC and ERPF during AngII infusion exceeded those during AngI (P<0.05). After cessation of either infusion, AngII concentrations, MAP, ERPF and Aldo returned to baseline levels within 1 h. Renin, however, was still significantly inhibited at that time (P<0.05). Catecholamines remained virtually unchanged during all experiments. Conclusions: Our data show that AngI and AngII have similar effects on blood pressure and Aldo, but they differ in their renal effects. The latter may be due to a low renal capacity to convert AngI. The prolonged inhibition of renin release after cessation of the infusions may be caused by reduced renin mRNA expression or by accumulation of AngII in the kidney.

KEYWORDS Man; Angiotensin I; Angiotensin II; Renal hemodynamics; Renin


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