Critical role of extracellular calcium in vanadate-induced renal vasoconstriction.

Abstract

Intra-arterial infusion of vanadate (VO4) in dogs produces a reduction in renal blood flow (RBF), glomerular filtration rate (GFR), urine flow (V), and the fractional excretion of sodium (FENa+). To evaluate the role of Ca2+ in these changes VO4 was infused into the renal artery in the presence of the calcium antagonists trifluoperazine (TFP), verapamil, or EGTA. TFP inhibited the effect of VO4 on RBF (TFP + VO4:64.1, VO4:38.5 ml/min; P less than 0.05), GFR (TFP + VO4:22.9, VO4:9.3, ml/min; P less than 0.05) and V (TFP + VO4: 0.80, VO4: 0.38 ml/min; P less than 0.05) without changing FENa+ (TFP + VO4: 3.8, VO4: 3.2%). Similar changes were obtained with verapamil as well as with EGTA. Furthermore thyroparathyroidectomy (TPTX) decreased serum calcium (control: 8.78, TPTX: 4.98 mg/100 ml; P less than 0.05) and blunted the effects of VO4 on renal hemodynamics. Reestablishing normal serum Ca2+ by an intra-arterial infusion of CaCl2 elicited the VO4 effects of vasoconstriction and decreased GFR; V was not affected and FENa+ rose. The data support the idea that influx of extracellular calcium into smooth muscle cells mediates the hemodynamic effects of VO4 in the dog.