@article{oai:niigata-u.repo.nii.ac.jp:00020821,
 author = {水戸, 元子},
 issue = {8},
 journal = {新潟医学会雑誌, 新潟医学会雑誌},
 month = {Aug},
 note = {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.},
 pages = {787--795},
 title = {アドレナリン作動性α_1-受容体刺激によるラット大動脈平滑筋の収縮 : 外液Na^+濃度依存性について},
 volume = {106},
 year = {1992}
}