Central Infusion of Aldosterone Increases Blood Pressure by Mechanisms Independent of Na Retention

Abstract

Experiments were performed to test the hypothesis that Na retention and Na in the diet are not required to initiate central aldosterone induced hypertension. Rats were fed either standard rat chow or Na-deficient diet and infused intracerebroventricularly (i.c.v.) with aldosterone (28 ng/h) dissolved in artificial cerebrospinal fluid (vehicle) or vehicle alone. In Na-replete rats the central infusion of aldosterone did not promote Na or water retention, prior to increases in systolic blood pressure (SBP). Infusion of aldosterone in Na-deficient rats also initiated a rise in SBP, although the response was delayed. In neither group of rats did aldosterone infusion significantly change plasma Na, K, renin, norepinephrine (NE) or vasopressin (AVP) concentrations. There was no significant increase in plasma aldosterone concentration in Na replete rats centrally infused with aldosterone. Infusion of vehicle had no effect on SBP. We conclude that central aldosterone infusion initiates an increase in blood pressure by a mechanism independent of Na retention. Furthermore, increased concentrations of systemic renin, vasopressin, and activation of the sympathetic nervous system do not appear to be involved in maintaining hypertension.

Chronic central infusion of aldosterone leads to sympathetic hyperreactivity and hypertension in Dahl S but not Dahl R rats

“…However, intracerebroventricular aldosterone at 25-28 ng/h for 2 wk has no effects on parameters, such as hematocrit, plasma electrolytes, plasma concentrations of renin, vasopressin or aldosterone, or water intake in Sprague Dawley (31) or Wistar (the present study and Ref. 36) rats.…”

“…This impairment is likely due to the aldosterone-induced activation of brain OLC and the brain RAS (17). Although intracerebroventricular aldosterone at 22.5 ng/h unlikely has direct peripheral effects (31,35), one cannot exclude indirect peripheral mechanisms contributing to baroreflex desensitization. In the present study, no parameter of resting sympathetic activity per se was measured.…”

“…36) rats. Intracerebroventricular aldosterone induces hypertension even in rats fed a Na ϩ -deficient diet (31). In addition, increased plasma vasopressin may sensitize the arterial baroreflex (14).…”

“…This dose of aldosterone was based on previous studies (31,36) in which in Wistar and Sprague Dawley rats intracerebroventricular aldosterone increased BP, sympathetic activity, and brain OLC but had no demonstrable effects on plasma electrolytes, renin, vasopressin, or aldosterone. This rate of infusion is ineffective when given systemically (8,31). Previous studies (2, 36) using up to 0.5% ethanol in aCSF as vehicle reported no effects on growth or neurological behavior.…”

The new biology of aldosterone

“…manner to the rat brain at low doses that have no effects if given subcutaneously. Aldosterone, over a 4-5-week period, produced sustained dose-responsive increases in systemic blood pressure within 2 weeks, which appear to be independent of changes in sodium handling (Kageyama & Bravo 1988, Peysner et al 1990). Concomitant i.c.v.…”