Effects of antihypertensive drugs on autoregulation of renal blood flow and glomerular capillary pressure in shr. Kvam, Fred Ivan, Jarle Ofstad, and Bjarne M. Iversen. Renal Research Group, Medical Department A, University of Bergen, Bergen, Norway.
APStracts 5:0073F, 1998.
The relationship between systemic blood pressure and glomerular capillary pressure (PGC) in SHR during treatment with antihypertensive drugs is still unclear. The effects of an angiotensin converting enzyme inhibitor (enalapril), two calcium channel antagonists (nifedipine, verapamil) and a [alpha]1-receptor blocker (doxazosin) on renal blood flow (RBF) autoregulation, PGC and renal segmental resistances was therefore studied in the spontaneously hypertensive rat (SHR). Recordings of RBF autoregulation were done before and 30 min after iv. infusion of the different drugs, and PGC was thereafter measured with stop-flow technic. 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 (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), while PGC after enalpril 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. 

Received 7 April 1997; accepted in final form 11 March 1998.
APS Manuscript Number F115-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 6 April 1998