Cardiac output and renal function during insulin-hypertension in sprague-dawley rats. Brands, Michael W., William F. Lee, Henry L. Keen, Magdalena Alonso -Galicia, Dion H. Zappe, and John E. Hall. Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216-4505 U.S.A.
APStracts 3:0046R, 1996.
Hyperinsulinemia has been reported to cause hypertension in rats, however, the renal and hemodynamic mechanisms for the rise in blood pressure are not known. In this study, changes in renal function, cardiac output, and total peripheral resistance were monitored to assess the hemodynamic mechanisms underlying the hypertensive response to insulin in rats. Eight rats (350 g), were instrumented with a Transonic flow probe on the ascending aorta and with abdominal aortic and femoral vein catheters. After recovery and a 4-day control period, a 7-day insulin infusion was begun (1.5 mU/kg/min, i.v.) together with glucose (22 mg/kg/min, i.v.) to prevent hypoglycemia. Cardiac output (CO), total peripheral resistance (TPR), mean arterial pressure (MAP), and heart rate were measured 24 hrs/day. MAP 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 after starting insulin infusion, averaging 94+4% of the control value of 121+7 ml/min. This decrease was not statistically significant with analysis of variance and was associated with a tendency for stroke volume to decrease during insulin infusion, from 0.314+0.021 to 0.287+0.031 ml. Heart rate did not change significantly from the control value of 384+8 bpm. Total peripheral resistance increased significantly to 122+11% of control by day 7. Renal hemodynamics were measured in 5 rats, and GFR 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 insulin-infusion periods, respectively, and no significant change in sodium balance was measured. These results indicate that insulin-hypertension in rats is initiated by an increase in total peripheral resistance, rather than by increased cardiac output. 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. 

Received 4 October 1995; accepted in final form 6 February 1996.
APS Manuscript Number R625-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 14 February 96