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AVP reduces transepithelial resistance across IMCD cell monolayers.
D R Mishler1, J A Kraut, G T Nagami
1Medical Service, Veterans Administration Medical Center, West Los Angeles 90073.
The American Journal of Physiology
|June 1, 1990
Summary
Arginine vasopressin (AVP) reduces inner medullary collecting duct (IMCD) cell resistance, suggesting amiloride-sensitive channels mediate its action. This effect is independent of cyclic AMP or intracellular calcium changes.
Area of Science:
- Nephrology
- Cell Physiology
- Molecular Endocrinology
Background:
- The inner medullary collecting duct (IMCD) is a key site for arginine vasopressin (AVP) action in regulating water balance.
- Understanding AVP's mechanism in the IMCD is crucial for comprehending renal physiology.
Purpose of the Study:
- To investigate the cellular mechanisms by which AVP modulates transepithelial resistance in cultured rat IMCD cells.
- To determine the roles of ion channels, cyclic AMP (cAMP), and intracellular calcium ([Ca2+]i) in AVP's action.
Main Methods:
- Cultured rat IMCD cells grown on permeable supports were used to measure transepithelial resistance.
- AVP, amiloride, forskolin, 8-bromo-cAMP, and ionomycin were applied to assess their effects.
- Intracellular calcium levels were measured using fura-2 fluorescence.
Main Results:
- AVP significantly decreased IMCD cell resistance, an effect reversible by amiloride.
- Trypsin treatment of the apical surface prevented the AVP-induced resistance fall, indicating protein involvement.
- Neither cAMP modulation nor AVP-induced changes in [Ca2+]i correlated with the observed resistance changes.
Conclusions:
- AVP likely acts through amiloride-sensitive apical channels in the IMCD.
- The AVP-induced decrease in resistance is independent of cAMP and intracellular calcium signaling pathways.
- These findings elucidate a novel aspect of AVP's action in renal water reabsorption.