Antihypertensive Effect of Prolonged Blockade of Angiotensin Formation in Benign and Malignant, one- and two-Kidney Goldblatt Hypertensive Rats

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Abstract
The effect of chronic inhibition of angiotensin II formation was investigated in 4 groups of hypertensive rats. Benign hypertension was produced by placing a 0.25 mm-diameter silver clip on the renal artery; a 0.20 mm clip was used to create malignant hypertension. A 2 kidney model had a clip plus intact contralateral kidney and a 1-kidney model had a clip plus contralateral nephrectomy. Benign and malignant groups were prepared in both the 1 kidney and 2 kidney variations. Converting enzyme inhibitor (SQ 14,225 [captopril]) was given to these 4 groups for 1 wk in drinking H2O and average intake ranged 33-77 mg/day. The 2 malignant groups had the highest plasma renin activities and they showed a precipitous fall in arterial pressure in the first 24 h of inhibition of angiotensin formation. All groups showed an additional slow decline in pressure during the remaining 6 days of inhibition. Changes in heart rate and Na excretion were variable but heart rate decreased during inhibition. Arterial pressure did not become normal with inhibition in either of the 1-kidney models: decreases to 126 and 132 mmHg were observed in the benign and malignant groups respectively. Of the malignant 1 kidney animals 3 became uremic with inhibition and 1 died before inhibition was discontinued. Arterial pressure was reduced to normal pressure (95 mmHg) after 1 wk of inhibition in both the benign and malignant 2-kidney models. It appears that normal pressure was restored in the 2-kidney model but not in the 1-kidney model because of the presence of the intact contralateral kidney. The physiological basis for this difference is not known, but changes in renal excretory function may be involved.