Related Experiment Videos
Electrogenic bicarbonate secretion by guinea pig gallbladder epithelium: apical membrane exit
C P Stewart1, J M Winterhager, K Heintze
1Abteilung Pharmakologie, Medizinischen Fakultät, Rheinisch-Westfälische Technische Hochschule Aachen, Federal Republic of Germany.
The American Journal of Physiology
|April 1, 1989
Summary
Adenosine 3
Area of Science:
- Physiology
- Cell Biology
- Biochemistry
Background:
- Guinea pig gallbladder epithelium secretes bicarbonate (HCO3-) via electroneutral mechanisms.
- Adenosine 3',5'-cyclic monophosphate (cAMP) alters this secretion to an electrogenic process.
Purpose of the Study:
- To investigate how cAMP transforms HCO3- secretion into an electrogenic process in guinea pig gallbladder epithelium.
- To elucidate the specific pathways and mechanisms involved in cAMP-mediated HCO3- transport.
Main Methods:
- Voltage-clamp, pH-stat, and microelectrode techniques were employed.
- Prostaglandin E1 (PGE1) was used to elevate intracellular cAMP levels.
- Ion substitutions and SITS (a Cl- -HCO3- exchange inhibitor) were utilized to probe transport mechanisms.
Main Results:
- PGE1 significantly increased short-circuit current (Isc) and net HCO3- secretion.
- Apical membrane depolarization and altered resistance ratios were observed with PGE1.
- Results indicated two distinct apical pathways for HCO3- exit: SITS-sensitive exchange for Cl- and a HCO3- conductive pathway.
Conclusions:
- cAMP-stimulated HCO3- secretion in guinea pig gallbladder epithelium involves both Cl- -HCO3- exchange and a separate HCO3- conductive pathway at the apical membrane.
- Cl- recycling via electrodiffusion plays a role in the SITS-sensitive component of secretion.
- These findings clarify the complex mechanisms of gallbladder HCO3- transport regulation.