Effect of plasma potassium on vascular response to pressor and depressor agents in dog kidney

The effect of plasma potassium concentration on the vascular response to the pressor agent angiotensin II (ANG II) and to the depressor agent prostaglandin E2 (PGE2) was investigated in dog kidney. Renal vascular reactivity to the vasoactive agents was assessed from the change in renal blood flow (RBF) after infusion of the agent into the renal artery. Plasma potassium concentration was increased by intravenous infusion of potassium L-aspartate solution. The vascular response to ANG II was attenuated when plasma potassium was increased, i.e. percent decrease in RBF produced by ANG II (26.1 +/- 8.4%) during potassium infusion (plasma K+, 5.68 +/- 0.31 mEq/L) was significantly lower than those (35.8 +/- 9.8, 30.4 +/- 7.8%) obtained in the control period (plasma K+, 3.60 +/- 0.40 mEq/L) and in the postinfusion period (plasma K+, 4.70 +/- 0.42 mEq/L). On the other hand, the vascular response to PGE2 showed a tendency to be potentiated by elevation of plasma potassium concentration, i.e. percent increases in RBF produced by PGE2 were 44.9 +/- 10.5% in the control period (plasma K+, 3.47 +/- 0.25 mEq/L), 50.5 +/- 6.8% during potassium infusion (plasma K+, 5.45 +/- 0.25 mEq/L) and 44.9 +/- 7.2% in the recovery period (plasma K+, 4.55 +/- 0.21 mEq/L). These changes in the vascular response obtained by elevation of plasma potassium appear to act towards lowering blood pressure.