Hormonal control of chloride secretion by canine tracheal epithelium: an electrophysiologic analysis.
A principal event in the stimulation of cyclic AMP-induced active C1 secretion across canine tracheal epithelium is an increase in the C1 permeability of the apical cell membrane. This permits C1 to leave the cell down its electrochemical potential difference across this barrier. C1 transport across the basolateral membrane appears to be nonconductive and may be mediated by NaC1 cotransport. Increased C1 entry across the basolateral membrane would enhance Na entry into the cell and secondarily stimulate Na extrusion from cell to submucosal solution. Increased Na-K-pump activity or an increase in the K permeability of the basolateral membrane may be responsible for the (Formula in text) reduction in basolateral membrane resistance that accompanies stimulation of C1 secretion. Analysis of the electromotive force across the apical cell membrane under conditions where C1 secretion is inhibited or stimulated provides reasonable estimates of intracellular Na and C1 activities for these conditions.
D000527:Alprostadil; D000818:Animals; D002712:Chlorides / Q000378:metabolism*; D000242:Cyclic AMP / Q000494:pharmacology; D004285:Dogs; D004837:Epinephrine / Q000494:pharmacology; D004848:Epithelium / Q000378:metabolism; D006728:Hormones / Q000494:pharmacology*; D008564:Membrane Potentials; D011458:Prostaglandins E / Q000494:pharmacology; D014132:Trachea / Q000378:metabolism* / Q000502:physiology
D002712:Chlorides; D006728:Hormones; D011458:Prostaglandins E; D000242:Cyclic AMP; D000527:Alprostadil; D004837:Epinephrine