A mechanism of contraction of the rat aortic smooth muscle by α_1-adrenoceptor stimulation : dependency on extracellular Na^+

Contraction of rat aortic smooth muscle by α_1-adrenoceptor stimulation was examined in relation to extracellular Na^+ concentration. Experiments were carried out in the presence of verapamil (Ver) 10^<-5>M to avoid the contribution of Ca^<2+> influx via voltage dependent Ca^<2+> channel (VDC). The contraction induced by phenylephrine (Phe) 10^<-6>M under this condition depended on the presence of Ca^<2+> in the extracellular space, suggesting that the Ca^<2+> influx from the extracellular space was indispensable for elicitation of contraction. The contraction was also dependent on the concentration of Na^+ in the extracellular space except for Na^+-free condition. Tonic component of the contraction constitued a plateau with low Na^+ concentrations, but showed a gradual increase with time with higher Na^+ concentrations. Dichlorobenzamil, a Na^+-Ca^<2+> exchange system inhibitor, attenuated this contraction. Noradrenaline (Nor) 10^<-6>M also showed an extracellular Na^+ dependent contraction, as Phe did. However, in the absence of Na^+, almost equal contraction to those observed in the presence of normal concentration of Na^+ was observed, suggesting the contribution of Ca^<2+> release from intracellular Ca^<2+> store. The contraction by Nor as well as by Phe were inhibited by H-7, a C-kinase inhibitor. These results suggest that, when α_1-adrenoceptor is stimulated, C-kinase is activated through formation of diacylglycerol and increases in Na^+ influx via Na^+-H^+ exchange system results. The accumulated Na^+, in turn, enhances Na^+-Ca^<2+> exchange leading to increases in Ca^<2+> influx