Fatty acid effects on angiotensin receptors

Saturated and unsaturated fatty acids were tested for their ability to inhibit specific binding of angiotensin to receptors in bovine adrenal glomerulosa and fasciculata cells, and homogenates of tissue from bovine adrenal and renal artery. Several naturally occurring fatty acids were inhibitory. The most potent fatty acids in the angiotensin-adrenal system were unsaturated C-18, C-20, and C-22 congeners, including oleic, linoleic, and arachidonic acids. These fatty acids inhibited angiotensin binding to adrenal glomerulosa cells by 50% at concentrations between 4 and 8 X 10(-6) M. Inhibition by linoleic acid was predominantly competitive, reducing receptor affinity by approximately 50% at the ID50 of the fatty acid. Renal artery binding sites were more sensitive than adrenal sites to linoleic, linolenic, and trans-vaccenic acids, but not to other fatty acids. Inhibition was not affected by indomethacin, nordihydroguaretic acid, or a guanosine triphosphate analogue. Fatty acids inhibiting the angiotensin-adrenal system had no effect on angiotensin antibody, adrenal receptors for atrial natriuretic factor, or myometrial receptors for bradykinin. Some fatty acids nonspecifically inhibited aldosterone production, blocking the response to angiotensin and substrate concentrations of corticosterone. This inhibition was apparently unrelated to effects on receptors. Albumin in the buffer partly neutralized the effects of added fatty acids. Pretreatment of fresh adrenal cells with albumin increased their ability to bind angiotensin. This was reversed by adding back the lipids absorbed to the albumin in the wash. Results suggest that endogenous fatty acids can regulate angiotensin receptors.