Na+-K+ exchanges in canine arterial and venous smooth muscle.

Abstract

The effect of altering active sodium transport was compared in the denervated canine femoral artery and saphenous vein, which respond differently to a variety of humoral and physical stimuli. Potassium removal and ouabain caused contractions that were larger in the vein than in the artery. Activation of sodium transport, by exposing sodium-loaded preparations to potassium, caused transient ouabain-sensitive relaxations in both blood vessels; depending on the contractile agonist used, this relaxant effect was comparable (BaCl2) in both preparations or was larger (norepinephrine) in the artery than in the vein. In both the artery and the vein, potassium-induced relaxations were larger during contractions evoked by BaCl2 than those caused by norepinephrine. In the vein, contractions caused by acetylcholine were inhibited by potassium to the same extent as those caused by BaCl2. These results 1) are compatible with a contribution of sodium transport mechanism to the control of cell membrane permeability for extracellular calcium in vascular smooth muscle; 2) suggest that active sodium-calcium exchanges are functionally more important in venous than in arterial smooth muscle; and 3) illustrate that the heterogeneous behavior of vascular smooth muscle of different anatomic origins reflects differences in excitation-contraction coupling.