血管内皮のNO産生系とCa^<2+>機構  [in Japanese] Endothelial NO production and Ca^<2+>  [in Japanese]

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Abstract

We examined the characteristics of Ca<SUP>2+</SUP> (Ca) signaling pathway for activation of endothelial NOS, with reference to 1) Ca entry triggered by depletion of stored Ca in the endothelium, 2) Ca entry channels in response to depletion of the stores, and 3) possible involvement of tyrosine kinase in the signaling pathway. In vascular endothelium, Ca-ATPase inhibitors depletes Ca stores by inhibiting Ca pump of the stores, which in turn triggers influx of Ca and activates cNOS and NO production. The channels through which Ca enter into the endothelial cells following agonist-stimulation or Ca-ATPase inhibitors seem to be of the SK&F96365-sensitive Ca channels. However, in the case of ACh, intracellularly stored Ca in part participates in NOS activation. Tyrosine kinase may be involved in the signaling pathway for Ca entry or Ca channel mechanism, because tyrosine kinase inhibitors inhibited effects of Ca-ATPase inhibitors. Triptoquinone A which has been reported to inhibit NOS induction primed by LPS/IL-1β attenuated endothelium-dependent relaxation induced by Ca-ATPase inhibitors and agonists, possibly via tyrosine kinase inhibition.

Journal

  • Folia Pharmacologica Japonica

    Folia Pharmacologica Japonica 106, 97-101, 1995-09-01

    The Japanese Pharmacological Society

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