Abstract

The extent and initial rate of potassium-induced relaxation of canine femoral and renal arteries were measured as a function of potassium concentration [K+]. Both parameters were greater in the renal artery at low [K+]; the dissociation constant for potassium of the femoral artery was greater than that of the renal artery. If potassium-induced relaxation reflects sodium pump activity, then these data indicate that the sodium pumps of the two arteries are different. When we repeated the above experiments in a lowered sodium medium, the rate and extent of potassium-induced relaxation and the apparent affinity for potassium increased in the femoral artery as predicted by kinetic models based on both isolated Na+-K+-ATPase and intact tissue. The same parameters in the renal artery, however, were unaffected by lowered sodium. These results and those presented in the companion paper [Am. J. Physiol. 245 (Heart Circ. Physiol. 14): H604-H609, 1983] can be interpreted to mean that potassium-induced relaxation does not accurately reflect sodium pump function in canine renal arteries.

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