PROPERTIES OF GLOMERULAR ANGIOTENSIN RECEPTORS IN ACUTE-RENAL-FAILURE IN THE RAT

  • 1 January 1983
    • journal article
    • research article
    • Vol. 102  (6) , 909-917
Abstract
Angiotensin (AII) binds to specific glomerular receptors to modulate glomerular filtration rate (GFR) in the normal kidney. To test the hypothesis that altered AII binding to the glomerulus may contribute to the decreased GFR in acute renal failure (ARF) the properties of glomerular AII receptors in models of ARF were studied. ARF was induced in rats by either HgCl2 (2.0 or 4.5 mg/kg) or 60 min renal ischemia. Outer cortical glomeruli isolated by sieving techniques were studied by equilibrium binding analysis. Scatchard analysis revealed 1 class of high-affinity receptors over a wide range of concentrations (10-11 to 10-8 M). Angiotensin binding to specific glomerular receptors was studied at 2 and 24 h after high-dose HgCl2. Glomerular AII receptor density was unchanged after mercuric chloride ARF [2 h: 783 .+-. 96 (N = 6), 24 h: 765 .+-. 69 (N = 4); normal control: 718 .+-. 64 (N = 9)]. The equilibrium affinity constant was unaltered after HgCl2 [2 h: 1.85 .+-. 0.28 .times. 108 M-1 (N = 6); 24 h: 1.80 .+-. 0.25 .times. 108 M-1 (N = 4); normal control: 2.02 .+-. 0.21 .times. 108 M-1 (N = 9)]. Plasma angiotensin II levels were elevated 2 h after HgCl2 (normal 16.2 .+-. 2.3 pg/ml; 2 h 47.6 .+-. 4.8) are returned to normal by 24 h (17.2 .+-. 2.4 pg/ml). Additional experiments performed 2 wk after low-dose HgCl2-induced ARF and at 24 h after unilateral renal artery clamp also demonstrated normal AII receptor affinity and density. Glomerular AII receptor binding is unaltered during the initiation, maintenance and recovery phases of ARF. Changes in the binding characteristics of glomerular AII receptors do not play a role in the pathogenesis of ARF.