CRITICAL ROLE OF EXTRACELLULAR CALCIUM IN VANADATE-INDUCED RENAL VASOCONSTRICTION

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 Na (FENa+). To evaluate the role of Ca2+ in these changes VO4 was infused into the renal artery in the presence of the Ca antagonists trifluoperazine (TFP), verapamil or EGTA [ethyleneglycol-bis(.beta.-aminoethyl ether)-N,N,N'',N'',-tetraacetic acid]. TFP inhibited the effect of VO4 on RBF (TFP + VO4: 64.1, VO4: 38.5 ml/min; P < 0.05), GFR (TFP + VO4: 22.9, VO4: 9.3, ml/min; P < 0.05) and V (TFP + VO4: 0.80, VO4: 0.38 ml/min; P < 0.05) without changing FENa+ (TFP + VO4: 3.8, VO4: 3.2%). Similar changes were obtained with verapamil as well as with EGTA. Thyroparathyroidectomy (TPTX) decreased serum Ca (control: 8.78, TPTX: 4.98 mg/100 ml; P < 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 Ca into smooth muscle cells mediates the hemodynamic effects of VO4 in the dog.