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  • 1
    Electronic Resource
    Electronic Resource
    Chloride secretion by canine tracheal epithelium: I. Role of intracellular cAMP levels (1982)
    Springer
    The journal of membrane biology 70 (1982), S. 217-226 
    Details
    ISSN: 1432-1424
    Keywords: tracheal epithelium ; cAMP ; prostaglandins ; short-circuit current ; chloride secretion ; secretogogues
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary We measured the short-circuit current (I sc) across canine tracheal epithelium and the intracellular cAMP levels of the surface epithelial cells in the same tissues to assess the role of cAMP as a mediator of electrogenic Cl secretion. Secretogogues fall into three classes: (i) epinephrine, prostaglandin (PG) E1, and theophylline increase bothI sc and cellular cAMP levels; (ii) PGF2α and calcium ionophore A23187, increaseI sc without affecting cell cAMP levels at the doses employed; and (iii) acetylcholine, histamine, and phenylephrine do not alter eitherI sc or cAMP levels. These findings indicate that: (i) increases in cAMP or Ca activity stimulate electrogenic Cl secretion by the columnar cells of the surface epithelium; (ii) cAMP mediates the effects of PGE1 and β-adrenergic agonists; (iii) a strict correlation between cAMP levels and Cl secretion rate is not apparent from spontaneous variations in these parameters or from dose-response relations ofI sc and cAMP to epinephrine concentration; and (iv) acetylcholine, histamine, and phenylephrine, agents that stimulate electrically-neutral NaCl secretion by submucosal glands, do not evoke cAMP-mediated, responses by the surface epithelium. Addition of 10−6 m indomethacin (or other prostaglandin synthesis inhibitors) to the mucosal solution decreasesI sc and cellular cAMP levels and reduces the release of PGE2 into the bathing media by 80%. Indomethacin does not interfere with the subsequent secretory response to PGE1. This suggests that endogenous prostaglandin production underlies the spontaneous secretion of Cl across canine tracheal epithelium under basal conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01870564
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  • 2
    Electronic Resource
    Electronic Resource
    Chloride secretion by canine tracheal epithelium: II. The cellular electrical potential profile (1982)
    Springer
    The journal of membrane biology 70 (1982), S. 227-238 
    Details
    ISSN: 1432-1424
    Keywords: tracheal epithelium ; microelectrodes ; membrane potentials ; membrane resistances ; chloride secretion ; secretagogues
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary We used intracellular microelectrode techniques to study the mechanisms responsible for Cl secretion by canine tracheal epithelium. Tissues were treated with indomethacin (10−6 m, added to the mucosal solution) to reduce the baseline rate of Cl secretion and then stimulated by addition of epinephrine (10−6 m) or prostaglandin E1 (10−6 m) to the submucosal solution. Three conclusions emerged from our findings: First, secretagogues enhance the rate of transepithelial Cl transport primarily by increasing apical membrane Cl permeability, since: (i) stimulation of secretion produced parallel decreases in transepithelial resistance (R t) and the membrane resistance ratioR a/Rb, whereR a andR b refer to the resistances of the apical and basolateral membranes; (ii) there was an inverse relation between the short-circuit current andR a/Rb; (iii) secretagogues depolarized the electrical potential difference across the apical membrane (ψa) and produced an equivalent hyperpolarization of the transepithelial electrical potential difference (ψ1) so that, in the steady-state, the basolateral membrane potential (ψb) was unchanged; and (iv) substitution of sulfate or gluconate for Cl in the bathing solutions prevented secretagogue-induced changes inR t, Ra/Rb, (ψa) and (ψ1). Second, Cl entry into the cell across the basolateral membrane appears to be electrically-neutral since omission of Cl from the submucosal solution had no effect on (ψb) and did not decreaseR a/Rb as would be expected if Cl entered the cell by a conductive process. Third, secretagogues decreaseR b. Approximately 20 sec after the onset of the secretory responseR a/Rb underwent a secondary increase whileR t continued to fall. The decrease inR b may reflect an increase in basolateral membrane K permeability.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01870565
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  • 3
    Electronic Resource
    Electronic Resource
    Adrenergic regulation of ion transport by primary cultures of canine tracheal epithelium: Cellular electrophysiology (1986)
    Springer
    The journal of membrane biology 91 (1986), S. 121-128 
    Details
    ISSN: 1432-1424
    Keywords: tracheal epithelium ; adrenergic agents ; chloride secretion ; chloride conductance ; potassium conductance ; electrophysiology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary We examined the effect of adrenergic agents on the cellular electrical properties of primary cultures of canine tracheal epithelium. Both isoproterenol and epinephrine stimulated Cl secretion, as evidenced by an increase in transepithelial voltage and a fall in transepithelial resistance. Moreover, both agents appear to increase the conductance of apical and basolateral membranes. However, the pattern of response was different. Isoproterenol initially depolarized apical voltage Ψ a and decreased the fractional resistance of the apical membranef R. These changes are consistent with an initial increase in apical Cl conductance. In contrast, epinephrine acutely hyperpolarized Ψ a and increasedf R, changes consistent with an initial increase in basolateral K conductance. Following the acute effect of epinephrine, Ψ a depolarized andf R decreased to values not significantly different from those observed with isoproterenol. The acute increase in basolateral K conductance produced by epinephrine appeared to result from stimulation of α adrenergic receptors because it was reproduced by addition of the α agonist phenylephrine, and blocked by the α antagonist phentolamine. The ability of prazosin but not yohimbine to block the acute epinephrine-induced increase in K permeability indicates the presence of α1 adrenergic receptors. The acute α adrenergic-induced increase in basolateral K conductance may be mediated by an increase in cell Ca because the response was mimicked by addition of the Ca ionophore A23187. In contrast, the response to isoproterenol was similar to that observed with addition of 8-bromo-cAMP and theophylline. These results indicate that both β and α adrenergic agents mediate the ion transport processes in canine tracheal epithelium. β adrenergic agents have their primary effect on the apical Cl conductance, probably via an increase in cAMP. α adrenergic agents exert their primary effect on the basolateral K conductance, possibly via an increase in cell Ca.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01925789
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