Central infusion of aldosterone increases blood pressure by mechanisms independent of Na retention

Clin Exp Hypertens A. 1990;12(3):399-414. doi: 10.3109/10641969009074742.

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aldosterone / blood
  • Aldosterone / pharmacology*
  • Animals
  • Biomechanical Phenomena
  • Blood Pressure / drug effects*
  • Brain / physiology*
  • Circadian Rhythm
  • Diet, Sodium-Restricted
  • Injections, Intraventricular
  • Male
  • Norepinephrine / blood
  • Osmolar Concentration
  • Rats
  • Rats, Inbred Strains
  • Renin / blood
  • Sodium / metabolism*
  • Vasopressins / blood

Substances

  • Vasopressins
  • Aldosterone
  • Sodium
  • Renin
  • Norepinephrine