Permissive role of alpha-tocopherol in the stimulation of aldosterone by sodium depletion in the guinea pig.

Abstract

To investigate the role of vitamin E in aldosterone synthesis, in vivo and in vitro studies were done in alpha-tocopherol-depleted guinea pigs. Seventy-one days of low vitamin E intake ( < 5 mg/kg feed) reduced the concentration of alpha-tocopherol in serum, liver and adrenals to low levels with no signs of hypovitaminosis. Aldosterone secretion was stimulated by 15 days on a low sodium diet (200 mg/kg feed) in controls and vitamin E-depleted animals. Sodium depletion in controls stimulated plasma aldosterone by 335%. Vitamin E depletion reduced the stimulation of plasma aldosterone to only 112% (p < 0.05). In vitro aldosterone secretion by adrenal cells from sodium-depleted animals was 252% higher than secretion by cells from controls. This enhancement of in vitro aldosterone secretion following in vivo sodium depletion was abolished completely by combined in vivo vitamin E and sodium depletion (p < 0.05). No significant differences between groups were found for plasma renin activity, adrenocorticotrophin and serum potassium, suggesting that intra-adrenal mechanisms like damage by enhanced lipid peroxidation in alpha-tocopherol-depleted animals rather than changes in humoral aldosterone-regulating factors are the cause of the attenuated aldosterone response to sodium depletion.