Role of calcium and albumin in the autoregulation of renal perfusate flow

Abstract

The role of Ca and albumin on the perfusate flow in isolated perfused rat kindeys was investigated. The initial perfusion medium was Krebs-Hanseleit bicarbonate solution with 1.82 mM-Ca without albumin. Perfusate flow autoregulation occurred above 100 mmHg. Raising albumin concentration to 20 and 60 g/l abolished autoregulation and increased perfusate flow. Keeping ionized Ca at 1.82 mM restored autoregulation in medium containing 20 and 60 g albumin/l. In 60 g albumin/l autoregulation occurred at a significantly higher flow. A concentration of 1.82 mM-ionized Ca appears to be a critical level for autoregulation of flow in these experiments, for autoregulation was not obtained in 60 g albumin/l medium containing 1.80 mM-ionized Ca. Autoregulation occurred in medium containing 1.83 mM-ionized Ca but at a lower perfusate flow. Raising albumin concentration to 120 g/l increased perfusate flow from 14.6 .+-. 0.8 to 20.8 .+-. 0.7 ml/min .cntdot. g (n = 5, P < 0.01) in the presence of 1.82 mM-total Ca and from 11.6 .+-. 1.0 to 15.8 .+-. 0.7 ml/min .cntdot. g (n = 5, P < 0.01) in 1.82 mM-ionized Ca. The effect of raising albumin concentration was reversible. Removing the capsule from the kidneys abolished the increased flow in response to raising albumin concentration. Apparently, the mechanism for the autoregulation of renal perfusate flow in isolated perfused kidneys is critically dependent on an extremely narrow range of ionized Ca concentration in the perfusion medium, below this range, autoregulation is not achieved; above it, autoregulation is achieved but during intense vasoconstriction; raising albumin concentration in the perfusion medium increases perfusate flow and abolishes autoregulation by lowering extracellular ionized Ca and by raising intrarenal tissue pressure.