Enalapril prevents aortic hyperreactivity and remodelling in one-kidney, one-clip hypertensive rats without reducing arterial pressure

1. The present study was designed to evaluate the blood pressure-independen t effects of angiotensin-converting enzyme (ACE) inhibition on cardiovascul ar structure and function in one-kidney, one-clip (1K1C) hypertensive rats. 2. The study was conducted in four groups of rats: (i) uninephrectomized no rmotensive rats (1K); (ii) 1K1C hypertensive rats; (iii) 1K rats treated wi th enalapril; and (iv) 1K1C rats treated with enalapril. Enalapril treatmen t (20 mg/kg per day, p.o.) was started after surgery to induce hypertension or nephrectomy and continued for 5 weeks. 3. The increase in blood pressure of 1K1C rats was associated with activati on of cardiac and aortic, but not plasma, ACE activity and with hypertrophy of both heart and aorta. No difference in cardiac output and in vitro syst olic function was observed among the groups. Hypertrophied aorta isolated f rom 1K1C rats displayed increased sensitivity to phenylephrine (PE) and una ltered responses to both acetylcholine (ACh) and sodium nitroprusside compa red with the 1K group. 4. Enalapril treatment effectively inhibited plasma and tissue ACE activity in 1K1C and 1K rats. Enalapril did not prevent the development of hyperten sion and cardiac hypertrophy nor did it change haemodynamic parameters in 1 K1C rats. However, enalapril prevented the increase in aortic media thickne ss and cross-sectional area and restored the hypersensitivity to PE in aort ic rings of 1K1C rats. The endothelium-dependent response to ACh was enhanc ed by enalapril in the aorta of 1K but not 1K1C rats. 5. These results suggest a role for activated local angiotensin II generati on in aortic but not cardiac hypertrophy secondary to 1K1C hypertension.