Abstract
Contractility and tone of depolarized vascular smooth muscle depend quantitatively on the presence of Ca ions which are required for the activation of myofibrillar ATPase. Thus, vasoconstriction increases if the extracellular Ca concentration rises, whereas vasodilation is produced by Ca deficiency. Physiologically, a highly potent Ca-antagonistic action is exerted by H ions. Accordingly, the natural constrictor effect of Ca on vascular smooth muscle disappears as a direct consequence of acidosis produced by external H accumulation or by an intensified intracellular glycolytic activity as in hypoxia. Conversely, the Ca-dependent vascular tone is potentiated with increasing alkalinity. By this mechanism the rate of metabolic H production controls the blood flow independently of autonomic nerve regulation (Grün et al., 1972; Grün and Fleckenstein, 1972; Grün et al., 1973). H ions seem to compete with Ca for the same active sites both at the transmembrane Ca transport system and at the myofibrillar ATPase (Schädler, 1967).
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Fleckenstein, A., Nakayama, K., Fleckenstein-Grün, G., Byon, Y.K. (1976). Interactions of H Ions, Ca-Antagonistic Drugs and Cardiac Glycosides with Excitation-Contraction Coupling of Vascular Smooth Muscle. In: Betz, E. (eds) Ionic Actions on Vascular Smooth Muscle. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-66427-4_24
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