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.
D000818:Animals; D001011:Aorta / Q000378:metabolism; D001693:Biological Transport, Active / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism*; D005665:Furosemide / Q000494:pharmacology*; D006801:Humans; D008564:Membrane Potentials / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D011817:Rabbits
D002712:Chlorides; D005665:Furosemide