Different Mechanisms for the Activation of Vascular Smooth Muscle by Norepinephrine and Depolarization

혈관 평활근의 수축기전에 관한 연구

The activation mechanism of the sustained contractions induced by norepinephrine and K-depolarization was studied in renal vascular muscle. Helical strips of arterial muscle were prepared from rabbit renal arteries. All experiments were performed in Tris-buffered Tyrode solution which was aerated with 100% $O_2$ and kept at $35^{\circ}C$. Renal arterial muscles developed a contracture rapidly when exposed to a 40 mM K-Tyrode solution. In the absence of external $Ca^{2+}$, however, no K-contracture appeared. The contracture induced by K-depolarization was abolished by the treatment with $Ca^{2+}-antagonist\;(verapamil)$ or lanthanum $(La^{3+})$. From these results, it is obvious that K-contracture of renal arterial strip required $Ca^{2+}$ in the medium and this contracture was developed by the increased $Ca^{2+}-influx$ due to K-depolarization. Noradrenaline (5 mg/l) induced also a similar sustained contraction rapidly in all strips. Even on the K-contracture and in $Ca^{2+}-free$ Tyrode solution and also in the Tyrode solution pretreated with verapamil or $La^{3+}$, noradrenaline produced a contraction. However, the contraction in $Ca^{2+}-free$ Tyrode solution was not sustained and decreased gradually. The amplitude of noradrenaline-induced contracture was dependent on external $Ca^{2+}$; The contracture increased dose-dependently, but over 3 mM $Ca^{2+}$, decreased. The results of this experiment suggest that K-contracture was developed by an increased $Ca^{2+}-influx$ due to membrane depolarization, while noradrenaline-induced contracture was developed by both transmembrane $Ca^{2+}-influx$ and the mobilizaiton of cellular $Ca^{2+}$