Korean J Physiol Pharmacol.
2000 Apr;4(2):113-120.
Regulation of the contraction induced by emptying of intracellular Ca2+
stores in cat gastric smooth muscle
- Affiliations
-
- 1Department of Physiology, College of Medicine, Catholic University
of Korea, 505 Banpo-dong, Socho-gu, Seoul, South Korea.
- 2Department of Pathophysiolory, College of Pharmacy, Chung-Ang University,
Seoul 156-756, Korea.
Abstract
- To investigate the mechanism of smooth muscle contraction induced by
emptying of intracellular Ca2+ stores, we measured isometric
contraction and 45Ca2+ influx. CaCl2 increased Ca2+ store emptying-
induced contraction in dose-dependent manner, but phospholipase C
activity was not affected by the Ca2+ store emptying-induced
contraction. The contraction was inhibited by voltage-dependent Ca2+
channel antagonists dose dependently, but not by TMB-8 (intracellular
Ca2+ release blocker). Both PKC inhibitors (H-7 and staurosporine) and
tyrosine kinase inhibitors (genistein and methyl 2,5-dihydroxycinnamic
acid) significantly inhibited the contraction, but calmodulin
antagonists (W-7 and trifluoperazine) had no inhibitory effect on the
contraction. The combined inhibitory effects of protein kinase
inhibitors, H-7 and genistein, together with verapamil were greater
than that of each one alone. In Ca2+ store-emptied condition, 45Ca2+
influx was significantly inhibited by verapamil, H-7 or genistein but
not by trifluoperazine. However combined inhibitory effects of protein
kinase inhibitors, H-7 and genistein, together with verapamil were not
observed. Therefore, this kinase pathway may modulate the sensitivity
of contractile protein. These results suggest that contraction induced
by emptying of intracellular Ca2+ stores was mediated by influx of
extracellular Ca2+ through voltage-dependent Ca2+ channel, also protein
kinase C and/or tyrosine kinase pathway modulates the Ca2+ sensitivity
of contractile protein.