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

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