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AJP - Heart and Circulatory Physiology, Vol 246, Issue 4 608-H614, Copyright © 1984 by American Physiological Society
ARTICLES |
E. L. Schiffrin, J. Gutkowska and J. Genest
The effect of angiotensin II (ANG II) and deoxycorticosterone acetate (DOCA) on the density (Bmax) and affinity (Kd) of binding sites for 125I-ANG II was investigated in a particulate fraction prepared from rat mesenteric arteriolar arcades. Rats were infused with ANG II via Alzet osmotic minipumps at a dose of 200 ng X kg-1 X min-1 intraperitoneally or 60 and 200 ng X kg-1 X min-1 intravenously for 5 days. Bmax was 127 +/- 5 fmol/mg protein, and Kd was 0.8 +/- 0.1 nM in controls and was reduced significantly after the intraperitoneal infusion (111 +/- 10 fmol/mg) or the lower intravenous dose (111 +/- 9 fmol/mg), whereas after the higher intravenous dose Bmax did not change (144 +/- 14 fmol/mg). Kd was unaffected in all groups. Plasma renin activity (PRA) was reduced, and plasma ANG II increased in a dose-dependent fashion after ANG II infusion. Plasma aldosterone concentration increased only in the group infused with ANG II at 200 ng X kg-1 X min-1 intravenously (to 33.8 +/- 8.0 ng/dl from 11.6 +/- 3.4). In rats implanted subcutaneously with silicone rubber impregnated with DOCA, Bmax for 125I-ANG II was significantly increased (to 142 +/- 4 fmol/mg), whereas rats receiving 1% NaCl in their drinking water had no change in binding capacity, although PRA was lower in both groups. DOCA infusion, when combined with the intravenous dose of ANG II that reduced Bmax, antagonized this action of ANG II. DOCA infusion into sodium-depleted rats partially corrected the down-regulation of vascular ANG II receptors independent of changes in PRA.(ABSTRACT TRUNCATED AT 250 WORDS)
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