Abstract
The effects of monensin, a Na ionophore, on the muscle contraction and the movements of monovalent cations were investigated in rabbit aorta. Experiments were conducted in the presence of phentolamine (10(-6) M) to avoid the vasoactive effect of monensin due to the release of endogenous catecholamine. Both monensin (2 X 10(-5) M) and ouabain (2 X 10(-5) M), added separately, produced a small and slowly developing contraction, whereas simultaneous application of these agents produced more rapid and greater contraction. Verapamil (10(-6) M) decreased the contraction by 75%. Ouabain gradually increased cellular Na content. Monensin augmented the ouabain-induced Na increase. Further, the loss of cellular Na into Na deficient solution was enhanced by monensin. Low temperature (0.5 degrees C) inhibited the monensin-induced increase in Na permeability. The relaxation of noradrenaline-contraction induced by a K-readmission was inhibited by ouabain but not by monensin. These results suggest that monensin increases Na movement down its electrochemical gradient, augments cellular Na accumulation when the Na pump is inhibited by ouabain, and induces muscle contraction, and that the contraction induced by monensin and ouabain is mainly due to an increased Ca influx through voltage sensitive Ca channels.
Published Version
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