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Cardiovascular Research 1998 40(2):402-409; doi:10.1016/S0008-6363(98)00124-2
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Divergent effects of ACE-inhibition and calcium channel blockade on NO-activity in systemic and renal circulation in essential hypertension

Lioe-Ting Dijkhorst-Oei, Jaap J. Beutler, Erik S.G. Stroes, Hein A. Koomans and Ton J. Rabelink*

Department of Nephrology and Hypertension, University Hospital, Utrecht, The Netherlands

* Corresponding author. Tel.: +31 (30) 250 7329; Fax: +31 (30) 254 3492; E-mail: t.rabelink@digd.azu.nl

Objective: Nitric oxide is a vasodilating and blood pressure lowering substance. To investigate whether calcium antagonists or angiotensin-converting enzyme (ACE) inhibitors increase vascular nitric oxide activity, we assessed systemic and renal vascular sensitivity to nitric oxide synthase inhibition in hypertensives on and off medication. Methods: Ten essential hypertensive patients, aged 22–51 years, were studied 3 times: ≥4 weeks off medication, after 3 weeks treatment with enalapril 20 mg twice a day and after 3 weeks nifedipine 60 mg/day. Each time, 24-h blood pressure registration was performed, followed by a clearance study to obtain a 3-h dose-response curve for intravenously infused NG-monomethyl-L-arginine (L-NMMA, respectively 0.75, 1.5 and 3.0 mg/kg/h). Results: L-NMMA dose-dependently increased mean arterial pressure with 5±2 mmHg and systemic vascular resistance with 24±5% at maximum dose, whereas cardiac output decreased (all P<0.001). Enalapril and nifedipine treatment decreased blood pressure, while the L-NMMA-induced increase in systemic vascular resistance was potentiated (enalapril: 45±7% and nifedipine: 46±8%; both P<0.01). L-NMMA also dose-dependently decreased renal blood flow by 58±8% at maximum dose (P<0.001), but neither drug potentiated these effects. Conclusion: These results indicate that, in essential hypertensives, antihypertensive therapy with enalapril or nifedipine increases nitric oxide dependency of systemic vascular tone, which may play a role in the blood pressure lowering effect of these drugs. However, this phenomenon cannot be observed in the renal circulation, suggesting a different regulation of endothelium-dependent vasomotion in the hypertensive kidney.

KEYWORDS Essential hypertension; Nitric oxide; L-NMMA; Angiotensin; Converting enzyme inhibitor; Calcium channel blocker; Systemic vascular resistance; Renal hemodynamics


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