RENOVASCULAR HYPERTENSION AND INSULIN SENSITIVITY

We tested the hypothesis that the status of the renin-angiotensin-aldo sterone system affects insulin sensitivity. Insulin sensitivity (by th e euglycaemic insulin clamp technique) was measured in eight patients with angiographically proven renovascular hypertension and in eight no rmotensive subjects matched for age, gender, body mass index and gluco se tolerance. In the patients, insulin sensitivity was measured both a t baseline and following 7 days of ACE inhibition. Following glucose i ngestion, patients and controls showed similar insulin and glucose res ponses. Insulin infusion (7 pmol min(-1) kg(-1)) promoted similar gluc ose utilization in the hypertensives and normotensives: 24.8 +/- 2.3 v s. 26.0 +/- 3.0 mu mol min(-1) kg(-1) respectively. One week of ACE in hibition caused a 20 +/- 4 mmHg decrease in mean blood pressure and a 20 +/- 6% decrease in peripheral vascular resistance. Plasma angiotens in II concentrations dropped from 24.6 +/- 6.3 to 13.5 +/- 5.0 pg mL(- 1) (P < 0.05) and plasma aldosterone from 17 +/- 4 to 9 +/- 2 ng dL(-1 ) (P < 0.05), and plasma renin activity doubled (from 1.6 +/- 0.3 to 3 .4 +/- 1.7 ng mL(-1) h(-1), P < 0.02). Nevertheless, insulin sensitivi ty was unchanged (before, 24.8 +/- 2.3; after, 25.8 +/- 2.2 mu mol min (-1) kg(-1), P = Ns). During insulin infusion, forearm blood flow did not change from baseline in either set of studies. Also, the antinatri uretic (before, -26 +/- 18; after, -22 +/- 14%) and antikaliuretic (be fore: -36 +/- 13%, after: -39 +/- 11%) action of the hormone was unaff ected by the therapy. In conclusion, human renovascular hypertension i s not associated with insulin resistance. Furthermore, a selective, dr astic reduction of the renin-angiotensin-aldosterone system activity a nd vascular tone does not alter insulin action on glucose and electrol yte metabolism.