Evidence that monensin inhibits vasopressin‐stimulated water flow at an early step in the receptor‐adenylate cyclase sequence

doi:10.1111/j.1768-322X.1989.tb00811.x

Paper

Evidence that monensin inhibits vasopressin‐stimulated water flow at an early step in the receptor‐adenylate cyclase sequence

Published 1989 · N. Franki, B. Mosenkis, R. M. Hays

Biology of the Cell

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Abstract

Monensin, a highly selective sodium ionophore, inhibits vasopressin‐stimulated water flow in toad urinary bladder pretreated with naproxen, an inhibitor of prostaglandin synthesis. Inhibition is partially dependent on the presence of sodium in the serosal medium, but not on serosal calcium. We have found that monensin does not inhibit water flow generated by forskolin, cyclic AMP, or isobutyl methyl xanthine (MIX); indeed, an enhancement of water flow was seen following cAMP and MIX, as well as following 0.2 μM forskolin. Our findings suggest that monensin uncouples the vasopressin‐receptor‐G protein‐adenylate cyclase sequence at some early step, by a mechanism that remains unknown, but that may directly or indirectlyinvolve intracellular sodium.

In Vitro Study

Study Snapshot

Monensin inhibits vasopressin-stimulated water flow in the urinary bladder by uncoupling the receptor-adenylate cyclase sequence at an early step, potentially involving intracellular sodium.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Evidence that monensin inhibits vasopressin‐stimulated water flow at an early step in the receptor‐adenylate cyclase sequence

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References

Citations

Structural correlates of the transepithelial water transport.

Intercellular junctions, intramembrane particles, and actin filaments play crucial roles in transepithelial water transport, regulating fluid flow across epithelial cells.