The three mechanisms of intracellular chloride accumulation in vascular smooth muscle of human umbilical and placental arteries

Recordings of membrane potential (E-m) and intracellular [Cl-] ([Cl-](i)) w ere made from the smooth muscle of human umbilical and placental arteries, using double-barrelled, ion-sensitive microelectrodes. In both arteries, [C l-](i) was above equilibrium with E-m. In the umbilical artery, [C1-](i) wa s 33.8+/-0.9 mM (+/-SD, n=19) and E-m-54.9+/-1.3 mV and in the placental ar tery respectively 35.11+/-0.7 mM (n=17) and -50.6+/-0.9 mV. In both arterie s, [Cl-](i) was reduced and E-m hyperpolarised significantly by successive additions of 100 muM 4,4 ' -diisothiocyanatodihydrostilbene-2,2 ' -disulpho nic acid (DIDS), 10 muM bumetanide and 1 mM acetazolamide, thus revealing t he presence of Cl-/HCO3- exchange, (Na+K+Cl) cotransport and "pump III". In the presence of all three inhibitors, [Cl-](i) was in equilibrium with E-m . As in earlier studies on rat arterial smooth and cardiac muscle, pump III was unaffected by DIDS, bumetanide, metolazone and the removal of Na+, par tly inhibited by chlorothiazide and fully inhibited by ethacrynic acid. The results are discussed in terms of the possibility that of chloride accumul ating systems may regulate vasomotor tone in the foetoplacental unit.