Abstract
Enhanced calcium content in arterial smooth muscle cells and altered reactivity of coronary vessels to alkalinization have been reported in angina pectoris due to impaired motility of coronary arteries. An altered function of sodium-hydrogen exchange, a ubiquitous membrane transport system that links proton efflux to calcium drifts, may mediate these phenomena. Twenty patients with microvascular angina (stable effort angina, reversible perfusion defects during effort thallium 201 heart scintigraphy, and angiographically normal coronary arteries) were compared to 20 patients with stable effort angina due to coronary atherosclerosis and 20 healthy subjects. The sodium-hydrogen exchange was defined as the initial fraction of the amiloride-sensitive proton efflux from red cells with inhibited anion exchanger (pHi 6.00-6.05) into an Na(+)-containing medium (pHo 8.00-8.05). 12-0-tetradecanoylphorbol-13-acetate (TPA, 600 nmol.l-1) and staurosporine (100 nmol.l-1) were used as phosphorylation modulators in vitro. The mean red blood cell Na+/H+ exchange was increased in patients with microvascular angina (451 +/- 37 vs 142 +/- 17 and 124 +/- 21 umol H+.1 cells-1.min-1, P < 0.01). TPA and staurosporine abolished differences between the groups. Microvascular angina is associated with enhanced Na+/H+ exchange in erythrocytes, probably due to more extensive phosphorylation of the membrane antiporter sites.
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