ENALAPRIL DOES NOT PREVENT RENAL ARTERIAL HYPERTROPHY IN SPONTANEOUSLY HYPERTENSIVE RATS

Angiotensin-converting enzyme inhibitors prevent the development of ve ssel wall hypertrophy in same vascular beds in spontaneously hypertens ive rats (SHR), but their effects on hypertrophy of renal arterial ves sels have not been studied. We therefore used stereological techniques to study wall and lumen dimensions of the interlobular (cortical radi al) 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-fixe d 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 int erlobular arteries, the volume density of artery wall, wall-to-lumen r atio, and wall thickness in the untreated SHR were significantly great er 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 mu m, respective ly), but values in the SHR-E were similar to those in the untreated SH R (1.10+/-0.20X10(-3), 0.88+/-0.22, and 14.0+/-2.6 mu m, respectively) . For the arcuate arteries, wall thickness and volume density were sig nificantly greater in SHR than WKY (17.3+/-3.0 Versus 13.9+/-1.7 mu m and 1.63+/-0.51 versus 1.14+/-0.27X10(-3), respectively), and values i n the SHR-E (15.7+/-1.7 mu m and 1.69+/-0.50X10(-3), respectively) wer e not signif icantly different from those in SHR. Thus, enalapril trea tment did not prevent Vessel wall hypertrophy of both the interlobular and arcuate arteries in SHR despite the normalization of arterial pre ssure. These results suggest that renal arterial hypertrophy in SHR is not caused by either angiotensin II or elevated arterial pressure.