ArticleThe Journal of membrane biology1995
Hydrochlorothiazide action on the apical Cl-, Ca2+ and K+ conductances in rabbit gallbladder epithelium. Presence of an apamin-sensitive, Ca(2+)-activated K+ conductance.
Article in The Journal of membrane biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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3 authors at 1 institution in 1 country.
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Abstract
In the rabbit gallbladder epithelium, hydrochlorothiazide (HCTZ) was shown to inhibit the transepithelial NaCl transport and the apical Na(+)-Cl- symport, to depolarize the apical membrane potential and to enhance the cell-to-lumen Cl- backflux (radiochemically measured), this increase being SITS-sensitive. To better investigate the causes of the depolarization and the Cl- backflux increase, cells were punctured with conventional microelectrodes on the luminal side (incubation in bicarbonate-free saline at 27 degrees C) and the apical membrane potential (Vm) was studied either with prolonged single impalements or with a set of short multiple impalements. The maximal depolarization was of 3-4 mV and was reached with 2.5 x 10(-4) M HCTZ. It was significantly enhanced by reducing luminal Cl- concentration to 30 mM; it was abolished by SCN-, furosemide, SITS; it was insensitive to DPC. SITS converted the depolarization into a hyperpolarization of about 4 mV; this latter was apamin, nifedipine and verapamil sensitive. It was concluded that HCTZ concomitantly opens apical Cl- and (probably) Ca2+ conductances and, indirectly, a Ca(2+)-sensitive, apamin inhibitable K+ conductance: since the intracellular Cl- activity is maintained above the value predicted at the electrochemical equilibrium, the opening of the apical Cl- conductance depolarizes Vm and enhances Cl- backflux. In the presence of apamin or verapamil, to avoid the hyperpolarizing effects due to HCTZ, the depolarization elicited by this drug was fully developed (7-10 mV) and proved to be Ca2+ insensitive. On this basis and measuring the transepithelial resistance and the apical/basolateral resistance ratio, the Cl- conductance opened by HCTZ has been estimated and the Cl- backflux increase calculate: it proved to be in the order of that observed radiochemically. The importance of this Cl- leak to the lumen in the overall inhibition of the transepithelial NaCl transport by HCTZ has been evaluated.
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