INSULIN-INDUCED HYPERTENSION IN RATS DEPENDS ON AN INTACT RENIN-ANGIOTENSIN SYSTEM

This study tested the dependence of insulin-induced hypertension in ra ts on a functional renin-angiotensin system. Rats were instrumented wi th chronic artery and vein catheters and housed in metabolic cages. Af ter acclimation, 10 rats began receiving the angiotensin-converting en zyme inhibitor (ACEI) benazepril at 1.8 mg . kg(-1) . d(-1) via a cont inuous intravenous infusion that was maintained throughout the study; 8 control rats received vehicle. Four days after starting ACEI or vehi cle, all rats entered a 5-day control period that was followed by a 7- day insulin infusion at 1.5 mU . kg(-1) . min(-1). Glucose was coinfus ed at 22 mg . kg(-1) . min(-1) to prevent hypoglycemia. Insulin infusi on in control rats increased mean arterial pressure (MAP; measured 24 h/d) from an average of 101 +/- 1 to 113 +/- 2 mm Hg on day 1; MAP ave raged 110 +/- 1 mm Hg for the 7-day infusion period. Glomerular filtra tion rate decreased, although not significantly, from 2.7 +/- 0.1 to 2 .1 +/- 0.2 mL/min on day 3. Chronic ACEI decreased baseline MAP from a n average of 97 +/- 1 to 79 +/- 1 mm Hg and markedly attenuated the in crease in MAP during insulin. MAP averaged 81 +/- 1 mm Hg for the 7-da y period and increased significantly, to 85 +/- 2 mm Hg, only on day 3 . Likewise, the tendency for glomerular filtration rate to decrease wa s blunted. These results indicate that insulin-induced hypertension in rats depends on angiotensin II and suggest that a reduction in glomer ular filtration rate contributes to the shift in pressure natriuresis.