Angiotensin II regulates its receptor sites in the adrenal glomerulosa zone

Abstract

DURING sodium deficiency, adrenocortical sensitivity to angiotensin II is increased in several species^1–3. Following acute sodium restriction in the rat, adrenal receptor sites for angiotensin II show increased concentration and binding affinity, and aldosterone responses to angiotensin II are increased both in vivo and in vitro⁴. Since circulating renin and angiotensin II levels are elevated during sodium deficiency^2,3, these changes in the adrenal gland could be mediated by the trophic action of angiotensin II on the zona glomerulosa. Increased levels of catecholamines and trophic peptide hormones, such as luteinising hormone, have been shown to cause receptor loss and desensitisation of specific responses in their respective target cells^5–7. It is possible, however, that physiological elevations of blood angiotensin II concentration could exert the opposite effect in the adrenal zona glomerulosa, leading to enhanced receptor function and contributing to the increased adrenal sensitivity during sodium restriction. To determine whether angiotensin II modulates its own receptors as well as the aldosterone secretory response, we examined angiotensin II receptors and aldosterone production in the zona glomerulosa of rats following elevation of circulating angiotensin II levels. These studies have provided evidence that angiotensin II can regulate its own receptor sites as well as steroidogenic responsiveness in the adrenal glomerulosa cell.