A single mechanism to explain the effect of calcium on renal function.

It is known that calcium induces the formation of potent vasodilators in endothelial cells and vasoconstriction in smooth muscle cells, whereas in the renal parenchyma, it modulates sodium excretion through vascular and tubular mechanisms. Consequently, an increased concentration of calcium in renal circulation may induce a sequence of contrasting hemodynamics and excretory effects depending on the threshold of a particular mechanism that is first being stimulated. In order to identify this sequence of responses and their respective thresholds, we infused into the renal artery of anesthetized dogs progressively increasing doses of calcium gluconate that ranged from 1 to 400 micrograms/kg/min. The administration of 1, 10, and 100 micrograms/kg/min of calcium gluconate was followed by a significant increase in urinary excretion of PGE2 and 6-keto-PGF1 alpha and by a marked diuresis and natriuresis without altering renal blood flow (RBF) or glomerular filtration rate (GFR). Renin release was increased by 80% only during the infusion of the 10 micrograms/kg/min dose. The intrarenal infusion of a 400 micrograms/kg/min dose of calcium produced marked decreases in RBF and GFR, while urine sodium excretion (UNaV), UPGE2V, and U6-keto-PGF1 alpha V continued and were markedly elevated. During all these maneuvers, mean arterial pressure remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)