Evidence for furosemide-sensitive active chloride transport in vascular smooth muscle.

An inhibitor of Cl- transport, furosemide, interfered potently with the 36Cl steady state exchange in rabbit aortic tissue. On long-term incubation with furosemide, [Cl-]i decreased ECl increased, thereby approaching the resting membrane potential of vascular smooth muscle. Electrophysiological microelectrode studies on rabbit pulmonary arteries revealed a hyperpolarization of 5.5 mV in the presence of furosemide. These findings provide evidence for an inwardly directed chloride pump operating in vascular smooth muscle.