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KMID : 0368119930230010092
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Korean Circulation Journal
1993 Volume.23 No. 1 p.92 ~ p.103
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Effect of Carffeine on the Ca2+ Pool Affecting Contractility and Actomyosin ATPase Activity in Vascular Smooth Muscle of Rabbit
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김진민
이영호/문창현/강복순/강두희.
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Abstract
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Caffeine has been known to induce the contraction of rabbit aortic ring resulting from Ca2+ release from the intracellular stores. But in contrast, contraction of aortic ring inducd by depolarizing agents or agonist was reported to be suppressed
by
caffeine.
The present study was intended to examine the effect of caffeine on Ca2+ movement across the plasma membrane and actomyosin ATPase activity of vascular smooth muscle to elucidate the modes of action of caffeine on the vascular smooth muscle.
Aortic ring preparation were made from the rabbit thoracic aorta and the endothelial cells were removed from the ring by gentle rubbing. The contractilty of the aortic ring was measured under varying conditions. and Ca2+ influx across the
membranes
of
the aortic ring was measured with Ca2+ sensitive electrode with and without caffeine and the effect of caffeine on actomyosin ATPase activity were measured by modified Hartshrone's method. 45Ca wash out curves with and without caffeine were
studied
by
Richard's method.
@ES The results were summarize as follows:
@EN 1) Caffeine inhibited the contractilty induced by norepinephrine, high K+, and histamine, but caffeine alone induced a transient contraction of vascular smooth muscle. The caffeine induced contraction was demonstrable even in the absence of
external
Ca2_.
2) Caffeine increased 45Ca efflux from vascular smooth muscle.
3) In the presence of propranolol, the inhibitory effect of caffeine on epinephrine induced contraction still persisted.
4) Caffeine decreased norepinephrine induced Ca2+ influx through the plasma membranes of aortic ring.
5) Caffeine decreased the actomyosin ATPase activity of vascular smooth muscle.
From the above results, it is suggested that caffeine induces the contraction of vascular smooth muscle by release of Ca2+ from intracellular Ca2+ store, but inhibits drug-induced contraction by decrease of Ca2+ influx across the plasma membranes
and a
decreased Ca2+ sensitivity of contractile protein in vascular smooth muscle.
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KEYWORD
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