Effect of electrolyte transport on the response of arteriolar smooth muscle

The purpose of this article is to discuss the manner in which inhibitors of the Na-K pump may cause constriction of the peripheral vasculature. In aortic smooth muscle there is evidence that, as in cardiac muscle, inhibitors of the Na-K pump such as ouabain act by causing an increase in the intracellular sodium content (Nai), and hence an increase in the intracellular free calcium concentration (Cai) via a Na-Ca exchange mechanism in the plasma membrane. However, the available evidence indicates that in the peripheral vasculature raised Nai is not in itself sufficient to cause contraction, suggesting that in the vessels responsible for the determination of peripheral resistance Na-Ca exchange mechanisms are not of major importance in calcium metabolism. Further evidence presented here on the basis of our experiments with isolated 200-micron artery preparations supports indications that the ability of ouabain to potentiate the tone of such vessels is due primarily to actions of ouabain other than the increase in Nai it produces. The data are consistent with the action of ouabain in the peripheral vasculature being mainly due to its depolarizing effect.