Effect of Alterations in Dietary Potassium on the Pressor and Steroidogenic Effects of Angiotensins II and III*

Abstract

The effects of angiotensins II (AII) and III (AIII) on blood pressure, serum aldosterone and serum corticosterone were compared in conscious rats maintained on a low, normal or high dietary K intake. In the 3 groups of rats, both peptides caused dose-related increases in mean arterial pressure, with AIII being significantly less (P < 0.001) potent than AII. The pressor responses to the angiotensins were significantly reduced by alterations in dietary K. When compared to the normal K group, the low K intake resulted in an 82% (P < 0.01) reduction, while high K intake resulted in a 72% (P < 0.01) reduction in the pressor responses to the angiotensins. The basal blood pressure and the pressor responses to norepinephrine were unaltered by changes in dietary K. AII and AIII were of similar potency in stimulating aldosterone release in low, normal and high K groups. Low K reduced the basal aldosterone level and inhibited the aldosterone responses to both angiotensins by 65% when compared to the normal group (P < 0.01). High K increased the basal aldosterone level and potentiated the angiotensin-induced aldosterone release (P < 0.01). Basal serum corticosterone levels and its response to AII and AIII were not markedly influenced by changes in dietary K. Changes in dietary K selectively reduce the pressor effects of AII and AIII while also modulating their steroidogenic effects, i.e., low K reduces while high K enhances angiotensin-induced aldosterone release.