Human Platelet Angiotensin II Receptors: Regulation by the Circulating Angiotensin Level*

Abstract

Human platelets possess angiotensin II (All) receptors which increase in number in response to sodium loading, a response similar to that reported for animal smooth muscle and renal All receptors. In these studies, we studied platelet All binding (by Scatchard analysis of competitive binding curves) in normal subjects as they changed their dietary sodium intake from 200 to 10 to 200 meq/day. Binding capacity fell significantly after 24 h of sodium restriction and furosemide diuresis, declining to a nadir of 40% of the binding capacity found during sodium loading (from 23 to 10 fmol AII/10⁹ platelets). Binding increased again after 24 h of sodium loading. There were no significant changes in receptor affinity during either low or high salt intake. The binding changes were significantly inversely correlated with the changes in plasma All levels (r = −0.87), suggesting that AH itself is the regulator of the platelet All receptor. Short term increases in All level (by furosemide administration or All infusion) did not alter platelet All binding, indicating that the changes in platelet binding were not due simply to receptor occupancy changes. These results show that platelets have the capacity for dynamic rapid up- and downregulation of their All receptors and that these receptor changes are regulated by the plasma All level.