Intricate interaction between store-operated calcium entry and calcium-activated chloride channels in pulmonary artery smooth muscle cells.

Ca(2+)-activated Cl-() channels (Cl(Ca)) represent an important excitatory mechanism in vascular smooth muscle cells. Active accumulation of Cl-() by several classes of anion transporters results in an equilibrium potential for this ion about 30 mV more positive than the resting potential. Stimulation of Cl(Ca) channels leads to membrane depolarization, which enhances Ca(2+) entry through voltage-gated Ca(2+) channels and leads to vasoconstriction.