Properties of glomerular angiotensin receptors in acute renal failure in the rat.

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) we studied the properties of glomerular AII receptors in models of ARF. ARF was induced in rats by either mercuric chloride (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 one class of high-affinity receptors over a wide range of concentrations (10(-11)M to 10(-8)M). Angiotensin binding to specific glomerular receptors was studied at 2 and 24 hr after high-dose mercuric chloride. Glomerular AII receptor density was unchanged after mercuric chloride ARF [2 hr: 783 +/- 96 (N = 6), 24 hr: 765 +/- 69 (N = 4); normal control: 718 +/- 64 (N = 9)]. Likewise, the equilibrium affinity constant was unaltered after HgCl2 [2 hr: 1.85 +/- 0.28 X 10(8)M-1 (N = 6); 24 hr: 1.80 +/- 0.25 X 10(8)M-1 (N = 4); normal control: 2.02 +/- 0.21 X 10(8)M-1 N = 9)]. Plasma angiotensin II levels were elevated 2 hr after HgCl2 (normal 16.2 +/- 2.3 pg/ml; 2 hr 47.6 +/- 4.8) and returned to normal by 24 hr (17.2 +/- 2.4 pg/ml). Additional experiments performed 2 weeks after low-dose HgCl2-induced ARF and at 24 hr after unilateral renal artery clamp also demonstrated normal AII receptor affinity and density. These studies demonstrated that 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.