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AJP - Cell Physiology, Vol 253, Issue 6 C817-C827, Copyright © 1987 by American Physiological Society
ARTICLES |
Y. Takuwa, N. Takuwa and H. Rasmussen
Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut 06510.
The cytoplasmic free Ca2+ concentration in bovine tracheal smooth muscle strips was measured using aequorin. Carbachol induces a rapid rise in aequorin luminescence, which reaches a peak within 1-2 min and then falls to a plateau level in 5-6 min. This plateau gradually declines but remains significantly above the base-line value after 2 h. The initial Ca2+ transient is due to Ca2+ mobilization from an intracellular caffeine-sensitive pool. The plateau appears to be due to Ca2+ influx. Histamine or 5-hydroxytryptamine (serotonin) also induce a Ca2+ transient followed by a plateau phase which is lower than that induced by carbachol. The isometric tension generated by either of these two agonists shows a gradual decline in contrast to the sustained plateau seen in the carbachol-induced contraction. Extracellular high K+ induces a dose-dependent increase in aequorin luminescence that is totally due to Ca2+ influx across the plasma membrane and is greatly inhibited by a Ca2+-channel antagonist, nimodipine. These results suggest that two temporally and spatially different Ca2+-dependent mechanisms are involved in carbachol-induced tracheal smooth muscle contraction.
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