CARDIOVASCULAR HYPERTROPHY IN ONE-KIDNEY ONE-CLIP RENAL HYPERTENSIVE RATS - A ROLE FOR ANGIOTENSIN-II

Objective: To investigate the role of angiotensin II (Ang II) in cardi ovascular hypertrophy in the Goldblatt one-kidney, one dip (1-K,1C) re nal hypertensive rat. Methods: Six-week-old Wistar-Kyoto (WKY) rats un derwent uninephrectomy and left renal artery clipping. After surgery, rats were treated with perindopril, an angiotensin converting enzyme ( ACE) inhibitor, or losartan, an Ang II type 1 (AT(1)) receptor antagon ist, for 4 weeks. Untreated 1-K,1C Fats and uninephrectomized (sham) r ats served as controls. Results: The rise in systolic blood pressure i n the perindopril-treated and losartan-treated rats was not significan tly different from that in the untreated 1-K,1C group throughout the t reatment period. At 4 weeks after surgery the heart weight:body weight ratios of the untreated 1-K,1C and losartan-treated 1-K,1C groups wer e significantly greater than far sham-operated normotensive rats and h ypertensive perindopril-treated rats. The total number of smooth muscl e cells in the thoracic aortae of the 1-K,1C untreated, losartan-treat ed 1-K,1C and sham groups were similar. However, after treatment the a ortae of the perindopril-treated group contained significantly fewer s mooth muscle cells. The medial cross-sectional wall area and wall:lume n ratio were similar in the 1-K,1C untreated and perindopril-treated 1 -K,1C groups. Conclusion: These results suggest that Ang II, via its e ffects on cardiac and vascular AT(1) receptors, does not contribute to the development of cardiovascular hypertrophy in the 1-K,1C rat. Atte nuation of cardiac and vascular growth after ACE inhibition appears to be mediated by mechanisms independent of the actions of the renin-ang iotensin system.