Hypertension during chronic hyperinsulinemia in rats is not salt-sensitive.

Author:

Brands M W1,Hildebrandt D A1,Mizelle H L1,Hall J E1

Affiliation:

1. Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.

Abstract

The goal of this study was to examine the chronic blood pressure and renal actions of insulin in conscious rats and to determine whether the blood pressure response to insulin is salt-sensitive. The effects of chronic hyperinsulinemia were examined in three groups of Sprague-Dawley rats given low sodium (LS rats, 0.6 meq/day), normal sodium (NS rats, 3.0 meq/day), or high sodium (HS rats, 11.4 meq/day) intakes. After 5-7 days of acclimation and 4 days of control measurements, insulin was infused 24 hr/day (1.5 milliunit/kg/min i.v.) for 7 days, and euglycemia was maintained by infusion of glucose (22 mg/kg/min i.v.). Mean arterial pressure was recorded continuously 19 hr/day, using computerized techniques, from chronically implanted aortic catheters. Chronic insulin infusion increased arterial pressure similarly in the three groups of rats, from 91 +/- 2 to 104 +/- 4 mm Hg in LS rats (n = 6), from 86 +/- 2 to 104 +/- 4 mm Hg in NS rats (n = 5), and from 91 +/- 2 to 105 +/- 8 mm Hg in HS rats (n = 5). There were no significant changes in plasma renin activity or glucose concentration in any group during insulin infusion. Control sodium excretions were 0.5 +/- 0.1, 2.3 +/- 0.1, and 9.3 +/- 0.6 meq/day in LS, NS, and HS rats, respectively, and there were no significant changes in urinary sodium excretion or cumulative sodium balance during 7 days of insulin infusion in any of the groups. These observations indicate that chronic hyperinsulinemia in rats produced hypertension that was not salt-sensitive and not dependent on sodium retention or increased renin secretion. Moreover, insulin-induced hypertension was associated with a shift of renal pressure natriuresis, since sodium balance was maintained at elevated arterial pressures.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Internal Medicine

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