Regulation of vascular angiotensin II receptors in the rat during altered sodium intake.

Changes in sodium intake exert well-defined and opposite effects on adrenal and vascular responsiveness to angiotensin n (All). Whereas the adrenal glomerulosa zone becomes more sensitive to All during sodium restriction, vascular sensitivity to All is decreased during sodium restriction and increased by sodium loading. The extent to which regulation of smooth muscle All receptors is involved in such altered vascular responsiveness was examined by assay of 125I-AU binding in the mesenteric artery and urinary bladder of rats during low and high sodium intake. The All receptors of vascular smooth muscle were found to be similar to those of the mesenteric artery in terms of their binding properties and regulation by altered sodium intake. During sodium restriction, blood All was elevated and All receptor concentration was significantly decreased (by 40%) in both tissues. Conversely, sodium loading was accompanied by decreased blood All and an increase in smooth muscle All receptors. The changes in All binding during sodium restriction were not attributable to occupancy of receptors by endogenous An, and no effect on receptor affinity was observed at either extreme of sodium intake. Elevation of the circulating AD concentration within the physiological range by infusion of the octapeptide for 2–4 days decreased An receptor concentration in urinary bladder particles. These findings demonstrate that smooth muscle All receptors are regulated during altered sodium intake, at least partially via changes in the circulating All concentration, in a manner reciprocal to the adrenal glomerulosa receptors. Such modulation of vascular AH receptors by the renin-angiotensin system could be responsible both for the altered pressor responses that accompany changes in sodium balance and for the reduced vascular reactivity that occurs in patients with high levels of circulating All.