Force development of smooth muscle cells is directly regulated by the concentration of free calcium ions in the sarcoplasm, and the sarcoplasmic concentration of calcium ion can be modulated by electrogenic Na-K pump. The role of Na-K pump on vascular tone was studied in isolated rabbit renal artery. Helical strips of arterial muscle were prepared from left renal arteries. All experiments were performed in HCO<sub>3</sub>-buffered Tyrode solution which was aerated with 3%CO<sub>2</sub>-97% O<sub>2</sub> mixed gas and kept at 35℃. In some experiments, rabbit was injected intraperitoneally 18~24 hours prior to the experiments, with a large dose(5 mg/kg body wt) of reserpine, in order to eliminate the catecholamines present in intrinsic adrenergic nerve terminate. Treatment used in this experiment that inhibits Na-K pump was the exposure of strips to K-free Tyrode solution. Contractile response to K-free Tyrode solution developed slowly and the time required for maximum contracture was 20~30 minutes. This K-free contracture was rapidly relaxed by the addition of potassium to the bathing solution. No K-free contracture occurred in a Ca-free Tyrode solution. But contraction developed rapidly when calcium ion was added to the bathing solution after 30 minute exposure of the strip to Ca-free Tyrode solution. This contracture was completely inhibited by Ca-antagonist, verapamil. The K-free contracture was abolished by α-adrenergic blocker, phentolamine, as well as by the catecholamine depletion from adrenergic nerve terminals. Even in reserpinized strip, the exogenous norepinephrine-induced contraction in K-free Tyrode solution was rapidly suppressed by the addition of potassium ion. The results of this experiment suggest that K free contracture develops by norepinephrine release from adrenergic nerve terminals, while the relaxation of K-free contracture is induced by the activation of electrogenic Na-K pump.
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