Vascular angiotensin II receptors in renal and DOCA-salt hypertensive rats.

To determine the contribution of receptor number and affinity to changes in vascular reactivity to angiotensin II (AII) in hypertensive rats, we have investigated the binding of 125I-AII to a particulate fraction of the rat mesenteric artery of hypertensive rats. In two-kidney, one clip hypertensive rats, receptor concentration (Bmax) was 83 +/- 13 fmol/mg and the dissociation constant (Kd) 0.6 +/- 0.1 nM vs 75 +/- 5.3 fmol/mg and 0.6 +/- 0.1 nM in normotensive controls, although PRA was much higher in the former. Bmax was reduced in these hypertensive rats after sodium depletion, as in normal rats. One-kidney, one clip hypertensive rats (Bmax 88 +/- 17 fmol/mg, Kd 0.6 +/- 0.1 nM) did not differ from uninephrectomized control rats (96 +/- 9 fmol/mg, Kd 0.5 +/- 0.1 nM). In DOCA-salt hypertensive rats, binding capacity was increased (125 +/- 2 fmol/mg, Kd 0.7 +/- 0.0 nM) vs uninephrectomized salt-loaded rats (Bmax 95 +/- 6 fmol/mg, Kd 0.6 +/- 0.1 nM), although PRA was suppressed comparably in both groups. The salt-loaded rats did not differ from uninephrectomized controls drinking water. We conclude that changes in the circulating renin-angiotensin system do not explain all the variations in receptor number in hypertensive rats. Our results suggest a role of mineralocorticoids in the regulation of vascular AII receptors.