ISSN:
1432-2013
Keywords:
HCO3 secretion
;
Membrane potentials
;
Cell membrane ion permeabilities
;
Ouabain
;
Prostaglandin E1
;
Loperamide
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Loperamide inhibits PGE1-induced electrogenic HCO3 secretion in guinea-pig gallbladder. Underlying changes in epithelial cell membrane properties were investgated using intracellular microelectrode techniques in vitro. In the absence of PGE1, mucosal loperamide (10−4 mol/l) reversibly depolarized both cell membranes by ∼ 6 mV. The apparent ratio of membrane resistances (R a/R b) remained unchanged and so did voltage responses to luminal Cl removal and Na reduction. The depolarizing response to elevation of luminal K concentration from 5 to 76 mmol/l was decreased from 13 to 8 mV. In the presence of 1 PGE1, the apical membrane is mainly permeable to Cl and HCO3. Under these conditions, loperamide reduced membrane potentials by ∼ 10 mV,R a/R b remaining constant at ∼ 0.4. Effects on voltage responses to changes in luminal Na or K concentration were unchanged. Responses to luminal Cl removal (transient depolarization) were greatly enhanced (from 22 to 42 mV) as predictable from the fall in K permeability that hinders Cl efflux from cell into lumen. Less marked but significant effects were obtained with 10−5 mol/l (mucosal side) and serosal loperamide (10−4 mol/l). We suggest that loperamide inhibits electrogenic HCO3 secretion by reducing apical membrane K permeability. The resulting depolarization diminishes the driving force for conductive anion efflux from cell into lumen. This conclusion is supported by the ability of luminal K elevation to mimick loperamide inhibition of the secretory flux of HCO3 (pH-stat experiments).
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00584635
