| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1992: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Research Abstract |
In this study, the roles of plasmalemmal Ca^<2+> channels and sarcoplasmic reticulum (SR), intracellular Ca^<2+> stores, in the development of tension in vascular smooth muscle, especially in resistance vessels, were investigated. The major findings are as follws.
1) Regulation of cytoplasmic Ca^<2+> ([Ca^<2+>]i) by Ca^<2+> channel and SR.I analyzed the effects of ryanodine and cyclopiazonic acid, modifiers of SR functions, on [Ca^<2+>]i, mesured with fura-2, and the tension of rat mesenteric resistance arteries. The results suggest that SR plays as a buffer to decrease [Ca^<2+>]i at a resting state, while it amplifies a contraction by releasing Ca^<2+> when transmembrane Ca^<2+> influx increased.
2) Ca^<2+> entry pathways following activation of alpha1-adrenoceptor. When alpha1-adrenoceptors of resistance vassels was activated by low concentration of agonist, Ca^<2+> influx through voltage-dependent Ca^<2+> channel (VDC) was enhanced without any depolarization. This influx triggered Ca^<2+> release from SR.A high concentration of agonist caused depolarization, which in turn enhanced the Ca^<2+> influx through VDC.Besides this, Ca^<2+> entry through a pathway other than VDC also occurred. This entry was sensitive to K^+ channel blockers but not to dihydropyridine Ca^<2+> channel blockers.
3) Functions of ion channels in the hypertensive vessels. In vascular smooth muscles from spontaneously hypertensive rate voltage-dependent Ca^<2+> channels were active at the resting state, which produced an active tension and activated Ca^<2+>-activated K^+ channels. Increased Ca^<2+> influx provided more Ca^<2+> to SR, then increased Ca^<2+> release from SR.
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