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Am J Physiol Renal Physiol 275: F576-F584, 1998;
0363-6127/98 $5.00
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Vol. 275, Issue 4, F576-F584, October 1998

Effects of antihypertensive drugs on autoregulation of RBF and glomerular capillary pressure in SHR

Fred Ivan Kvam, Jarle Ofstad, and Bjarne M. Iversen

Renal Research Group, Medical Department A, University of Bergen, N-5021 Bergen, Norway

The relationship between systemic blood pressure and glomerular capillary pressure (Pgc) in spontaneously hypertensive rats (SHR) during treatment with antihypertensive drugs is still unclear. The effects of an angiotensin-converting enzyme inhibitor (enalapril), two calcium channel antagonists (nifedipine and verapamil), and an alpha 1-receptor blocker (doxazosin) on renal blood flow (RBF) autoregulation, Pgc, and renal segmental resistances were therefore studied in SHR. Recordings of RBF autoregulation were done before and 30 min after intravenous infusion of the different drugs, and Pgc was thereafter measured with the stop-flow technique. When the mean arterial pressure (MAP) was reduced to ~120 mmHg by infusions of doxazosin or enalapril, the lower pressure limit of RBF autoregulation was reduced significantly. Nifedipine or verapamil abolished RBF autoregulation. Doxazosin did not change Pgc (43.6 ± 1.4 vs. 46.7 ± 1.5 mmHg in controls, P > 0.5), enalapril lowered (41.3 ± 0.8 mmHg, P < 0.01), and the calcium channel antagonists increased Pgc [53.7 ± 1.4 mmHg (nifedipine) and 54.8 ± 1.2 mmHg (verapamil), P < 0.01]. When MAP was reduced to ~85 mmHg by drugs, Pgc was reduced to 43.3 ± 1.7 mmHg after nifedipine (P > 0.2 vs. control), whereas Pgc after enalapril was 38.5 ± 0.5 mmHg (P < 0.05 vs. control). Enalapril reduced Pgc mainly by reducing efferent resistance. During treatment with calcium channel antagonists, Pgc became strictly dependent on MAP. Monotherapy with nifedipine may increase Pgc and by this mechanism accelerate glomerulosclerosis if a strict blood pressure control is not obtained.

calcium channel antagonist; angiotensin-converting enzyme inhibitor; alpha 1-adrenergic receptor blocker; hypertension; renal micropuncture; renal hemodynamics; renal blood flow


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