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The study of cellular Ca2+ exchange in smooth muscle has been severely limited by extensive extracellular Ga2+ binding. This problem was solved by using La3+ to trap Ca2+ inside the cells while displacing extracellular bound Ca2+. It was then shown that cytoplasmic Ca2+ could be raised by Ca2+ influx during high K+ depolarization, Na+ elimination and high pH. Ca2+ influx was inhibited by other multivalent cations, local anaesthetics and low pH. In the rabbit aortae norepinephrine and angiotensin increase cytoplasmic Ca2+ by release from intracellular membrane surfaces. In this same smooth muscle relaxation is brought about by intracellular Ca2+ binding. Evidence from vascular, uterine and intestinal smooth muscle demonstrates that the large transmembrane Ca2+ gradient depends on cellular [ATP] but not on the Na+ gradient. ATP depletion abolishes the Ca2+ gradient by increasing Ca2+ influx.
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Breemen et al. (1973) studied this question.
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