This experiment was designed to investigate the effect of converting enzyme inhibition on functional and structural vascular alterations in one-kidney, one clip hypertensive rats and in normotensive rats. Starting 1 day before surgery, 100 mg/kg/day captopril was given chronically to half of the hypertensive and normotensive groups in their drinking water. With use of intravital microscopy in the cremaster muscle, arteriolar dimensions were measured 4 weeks later, both before and after topical application of 10~3 M adenosine. Mean blood pressure was 124 ±4 mm Hg in control rats and 103 ±5 mm Hg in captopril-treated control rats (p<0.05). Mean blood pressure was significantly elevated to 183±5 mm Hg in captopril-treated one-kidney, one clip hypertensive rats and 193 ±5 mm Hg in one-kidney, one clip hypertensive rats. With use of histological techniques, a marked reduction of medial-intimal area of the abdominal aorta was found in captopril-treated control rats (24%), and hypertrophy of the aortic wall in one-kidney, one clip hypertensive rats was decreased 26% by captopril. Structural diameter reductions occurred in large arterioles of the captopril-treated control and hypertensive groups and the nontreated hypertensive group. In spite of a significant increase in wall-to-lumen ratio of first-order arterioles in all captopril-treated rats, captopril decreased cross-sectional wall area of these vessels 37% in hypertensive and 20% in control rats, respectively. Measured by stereological techniques, small arteriolar density decreased 30% in captopril-treated hypertensive rats and 17% in captopril-treated control rats. Therefore, smaller arteriolar lumens, decreased aortic and arteriolar cross-sectional wall area, and arteriolar rarefaction after converting enzyme inhibition, in spite of rising or falling blood pressure, are evidence that vascular growth was inhibited in vivo. {Hypertension 1990;15:68-77) T he influence of angiotensin II (Ang II) on vascular structure has been widely studied. Ang II has been shown to stimulate DNA and protein synthesis in cardiovascular tissue 1 and induce hypertrophy without cellular proliferation in cultured rat aortic smooth muscle cells (SMCs) maintained in a defined serum-free medium.2 Ang II also increased growth rates and cell size in cultured human SMCs grown in the presence of serum. However, all of these were in vitro studies. In vivo, captopril not only lowered blood pressure, but was more effective than hydralazine and propranolol in preventing increases in aortic SMC content, medial SMC weight, and percentage of polyploid SMCs in spontaneously hypertensive rats (SHR).4 SMC volume was also reduced in captopril-treated SHR and Wistar-Kyoto (WKY) rats. 4 In mesenteric arteries, captopril induced a long-lasting decrease in wallto-lumen (W/L) ratio in SHR and simultaneously induced long-lasting decreases in myocardial and aortic wall hypertrophy that persisted up to 7 weeks after treatment withdrawal.5 Recently, converting enzyme inhibition in two-kidney, one clip hypertensiv...