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(Hypertension. 1995;25:335-342.)
© 1995 American Heart Association, Inc.

Articles

Enalapril Does Not Prevent Renal Arterial Hypertrophy in Spontaneously Hypertensive Rats

Michelle M. Kett; Daine Alcorn; John F. Bertram; Warwick P. Anderson

From the Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Victoria, and the Emily E.E. Stewart Renal Laboratory, Baker Medical Research Institute (W.P.A.), Prahran, Victoria, Australia.

Correspondence to Dr Warwick P. Anderson, Baker Medical Research Institute, Alfred Hospital, Commercial Rd, Prahran, Vic 3181, Australia.

Abstract Angiotensin-converting enzyme inhibitors prevent the development of vessel wall hypertrophy in some vascular beds in spontaneously hypertensive rats (SHR), but their effects on hypertrophy of renal arterial vessels have not been studied. We therefore used stereological techniques to study wall and lumen dimensions of the interlobular (cortical radial) and arcuate arteries in the kidneys of SHR (n=7), SHR treated from 4 to 10 weeks of age with enalapril (25 to 30 mg/kg per day; SHR-E, n=7), and Wistar-Kyoto rats (WKY, n=7). All kidneys were perfusion-fixed at 10 weeks. Systolic blood pressure was 199±9, 139±11, and 156±8 mm Hg in the SHR, SHR-E, and WKY groups, respectively. For the interlobular arteries, the volume density of artery wall, wall-to-lumen ratio, and wall thickness in the untreated SHR were significantly greater than in the WKY (0.84±0.09 versus 0.69±0.07x10^-3, 0.75±0.20 versus 0.53±0.08, and 13.6±3.3 versus 10.6±0.8 µm, respectively), but values in the SHR-E were similar to those in the untreated SHR (1.10±0.20x10^-3, 0.88±0.22, and 14.0±2.6 µm, respectively). For the arcuate arteries, wall thickness and volume density were significantly greater in SHR than WKY (17.3±3.0 versus 13.9±1.7 µm and 1.63±0.51 versus 1.14±0.27x10^-3, respectively), and values in the SHR-E (15.7±1.7 µm and 1.69±0.50x10^-3, respectively) were not significantly different from those in SHR. Thus, enalapril treatment did not prevent vessel wall hypertrophy of both the interlobular and arcuate arteries in SHR despite the normalization of arterial pressure. These results suggest that renal arterial hypertrophy in SHR is not caused by either angiotensin II or elevated arterial pressure.

Key Words: kidney • hypertension, renovascular • hypertrophy • angiotensin II • arteries

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