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Interaction of calcium and cyclooxygenase inhibitors on transport by the turtle and toad bladders
Abstract:
Agents or maneuvers which increase intracellular calcium, inhibit Na, H + and AVP-stimulated water transport by the turtle and toad bladders. The mechanism of the inhibitory effect remains incompletely defined. An increase in intracellular calcium has been shown to stimulate prostaglandin release in several tissues. Since prostaglandins are capable of altering transport we examined whether cyclooxygenase inhibition would alter the inhibitory effect of the high extracellular calcium, ionophore A23187, or carbachol on AVP-stimulated water flow in the toad bladder and on Na and H + transport measured as the short circuit current and reverse short circuit current respectively by the turtle bladder. Indomethacin or ibuprofen was used at a dose of 10(-6) M which has been shown to inhibit the release of endogenous prostaglandin. Pretreatment with indomethacin or with ibuprofen significantly decreased the inhibitory effect of high extracellular calcium, ionophore, or carbachol on AVP-stimulated water flow in the toad bladder. Pretreatment with indomethacin did not alter the inhibitory effect of the ionophore or carbachol on Na or H + transport by the turtle bladder. The data demonstrate that pretreatment with indomethacin or ibuprofen blunts the effect of agents which increase intracellular calcium on water transport but not on Na or H + transport. It is suggested that high intracellular calcium inhibits water transport via prostaglandin release whereas the inhibition of Na or H + transport is independent of prostaglandin.
Insights
Increasing intracellular calcium inhibits water transport via prostaglandin release, but not sodium or hydrogen transport. This study investigated the role of prostaglandins in calcium-mediated transport inhibition.
Area of Science:
- Physiology
- Cell Biology
- Biochemistry
Background:
- Intracellular calcium increases can inhibit water, sodium, and hydrogen transport in bladders.
- The precise mechanism for this inhibition is not fully understood.
- Prostaglandins, known to affect transport, may be involved in calcium-mediated inhibition.
Purpose of the Study:
- To investigate if cyclooxygenase inhibition affects the inhibitory impact of elevated intracellular calcium on transport.
- To determine if prostaglandin release mediates the inhibition of water, sodium, and hydrogen transport.
Main Methods:
- Using toad and turtle bladders to study transport.
- Administering agents that increase intracellular calcium (calcium, ionophore A23187, carbachol).
- Pretreating with cyclooxygenase inhibitors (indomethacin, ibuprofen) to block prostaglandin synthesis.
Main Results:
- Indomethacin and ibuprofen significantly reduced the inhibitory effect of calcium-increasing agents on AVP-stimulated water flow in toad bladders.
- These inhibitors did not affect the inhibition of sodium and hydrogen transport in turtle bladders.
- The data indicate that prostaglandin release mediates the inhibition of water transport but not sodium or hydrogen transport.
Conclusions:
- Elevated intracellular calcium inhibits water transport through prostaglandin release.
- The inhibition of sodium and hydrogen transport by increased intracellular calcium is independent of prostaglandins.
- This suggests distinct mechanisms for calcium's effect on water versus ion transport.