ENHANCED RED SELL SODIUM-HYDROGEN EXCHANGE IN MICROVASCULAR ANGINA

Objectives Enhanced calcium content in arterial smooth muscle cells an d altered reactivity of coronary vessels to alkalinization have been r eported in angina pectoris due to impaired motility of coronary arteri es. An altered function of sodium-hydrogen exchange, a ubiquitous memb rane transport system that links proton efflux to calcium drifts, may mediate these phenomena. Design and subjects Twenty patients with micr ovascular angina (stable effort angina, reversible perfusion defects d uring effort thallium 201 heart scintigraphy, and angiographically nor mal coronary arteries) were compared to 20 patients with stable effort angina due to coronary atherosclerosis and 20 healthy subjects. The s odium-hydrogen exchange was defined as the initial fraction of the ami loride-sensitive proton efflux from red cells with inhibited anion exc hanger (pHi 6.00-6.05) into an Na+-containing medium (pHo 8.00-8.05). 12-O-tetradecanoyl-phorbol-13-acetate (TPA, 600 nmol.l(-1)) and stauro sporine (100 nmol.l(-1)) were used as phosphorylation modulators. in v itro. Results The mean red blood cell Na+/H+ exchange was increased in patients with microvascular angina (451 +/- 37 vs 142 +/- 17 and 124 +/- 21 mu mol H+.1 cells(-1).min(-1), P<0.01). TPA and staurosporine a bolished differences between the groups. Conclusions Microvascular ang ina is associated with enhanced Na+/H+ exchange in erythrocytes, proba bly due to more extensive phosphorylation of the membrane antiporter s ites.