Caffeine-induced contraction in vascular smooth muscle.

Characteristics of caffeine-induced contraction were compared with those of high K+- and norepinephrine-induced contractions in order to evaluate the participation of the Ca++-induced Ca++-release (CCR) from storage site in the vascular smooth muscle of rabbit aorta. Caffeine induced a transient contraction in a solution without MgCl2. One mM Mg++ selectively inhibited the caffeine-induced contraction. Two mM procaine inhibited the contractions induced by caffeine, high K+ and norepinephrine. One mM lidocaine and low temperature (23 degrees C) inhibited both high K+- and norepinephrine-induced contractions but rather potentiated the caffeine-induced contraction. Simultaneous addition of 10(-6) M verapamil and 10(-5) M sodium nitroprusside inhibited both high K+- and norepinephrine-induced contractions, but not the caffeine-induced contraction. In a Ca++-free solution, both caffeine and norepinephrine induced transient contractions. Norepinephrine-induced transient contraction was more strongly inhibited than caffeine-induced contraction by 2 mM procaine and 1 mM lidocaine, whereas 5 mM Mg++ inhibited only the caffeine-induced contraction. In sarcoplasmic reticulum of skeletal muscle, it has been shown that the CCR is activated by caffeine and inhibited by procaine, but not by lidocaine and low temperature. Although Mg++ is an inhibitor of CCR, changes in extracellular Mg++ concentrations do not seem to readily modify the intracellular Mg++ concentration in the intact smooth muscle, and the inhibitory effect of Mg++ on caffeine-induced contraction may not be attributable to the direct effect on sarcoplasmic reticulum. These results suggest that the CCR plays an important role in the contraction induced by caffeine but not in the contractions induced by high K+ and norepinephrine in the vascular smooth muscle of rabbit aorta.