CARDIAC-OUTPUT AND RENAL-FUNCTION DURING INSULIN HYPERTENSION IN SPRAGUE-DAWLEY RATS

Hyperinsulinemia has been reported to cause hypertension in rats; howe ver, the renal and hemodynamic mechanisms are not known. In this study , changes in renal function, cardiac output (GO), and total peripheral resistance (TPR) were measured during chronic insulin infusion in eig ht rats (similar to 350 g). After a 4-day control period, a 7-day insu lin infusion was begun (1.5 mU . kg(-1). min(-1) iv), together with gl ucose (22 mg . kg(-1). min(-1) iv) to prevent hypoglycemia. Mean arter ial pressure (MAP), CO, TPR, and heart rate were measured 24 h/day. MA P increased from 92 +/- 1 to 100 +/- 2 mmHg on day 1 and was 108 +/- 4 mmHg by day 7 of insulin. CO tended to decrease during insulin infusi on, although not significantly, averaging 94 +/- 4% of the control val ue of 121 +/- 7 ml/min. Heart rate did not change significantly from t he control value of 384 +/- 8 beats/min. TPR increased significantly t o 122 +/- 11% of control by day 7. In five rats, glomerular filtration rate and effective renal plasma flow decreased to 73 +/- 4 and 66 +/- 5% of control, respectively, during insulin. Urinary sodium excretion averaged 2.6 +/- 0.1 and 2.7 +/- 0.1 meq/day during the control and i nsulin-infusion periods, respectively. These results indicate that ins ulin hypertension in rats is initiated by an increase in TPR rather th an by increased CO. Also, the fact that sodium balance was maintained at elevated arterial pressure suggests that the ability of the kidneys to excrete sodium was impaired chronically during insulin infusion.