## Abstract

The study of cellular Ca<latex>$^{2+}$</latex> exchange in smooth muscle has been severely limited by extensive extra-cellular Ca<latex>$^{2+}$</latex> binding. This problem was solved by using La<latex>$^{3+}$</latex> to trap Ca<latex>$^{2+}$</latex> inside the cells while displacing extracellular bound Ca<latex>$^{2+}$</latex>. It was then shown that cytoplasmic Ca<latex>$^{2+}$</latex> could be raised by Ca<latex>$^{2+}$</latex> influx during high K<latex>$^+$</latex> depolarization, Na<latex>$^+$</latex> elimination and high pH. Ca<latex>$^{2+}$</latex> influx was inhibited by other multivalent cations, local anaesthetics and low pH. In the rabbit aortae norepinephrine and angiotensin increase cytoplasmic Ca<latex>$^{2+}$</latex> by release from intra-cellular membrane surfaces. In this same smooth muscle relaxation is brought about by intracellular Ca<latex>$^{2+}$</latex> binding. Evidence from vascular, uterine and intestinal smooth muscle demonstrates that the large transmembrane Ca<latex>$^{2+}$</latex> gradient depends on cellular [ATP] but not on the Na<latex>$^+$</latex> gradient. ATP depletion abolishes the Ca<latex>$^{2+}$</latex> gradient by increasing Ca<latex>$^{2+}$</latex> influx.