Effects of Ca 2+ channel blockers on amiloride-sensitive Na + permeable channels and Na + transport in fetal rat alveolar type II epithelium
Biochemical Pharmacology, ISSN: 0006-2952, Vol: 63, Issue: 8, Page: 1547-1552
2002
- 9Citations
- 6Captures
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Metrics Details
- Citations9
- Citation Indexes9
- CrossRef9
- Captures6
- Readers6
Article Description
A β-adrenergic agonist (β-agonist), terbutaline, stimulated amiloride-sensitive Na + absorption in fetal rat alveolar type II epithelium, contributing to the clearance of lung fluid. Cytosolic Ca 2+ plays an important role in terbutaline-stimulated Na + absorption, since Ca 2+ -activated, amiloride-sensitive Na + -permeable channels are involved in transcellular Na + absorption and terbutaline stably elevates the cytosolic Ca 2+ concentration by stimulating Ca 2+ influx. Therefore, we studied whether Ca 2+ channel blockers (Ni 2+, verapamil, and nifedipine) affect terbutaline-stimulated transcellular Na + absorption. Ni 2+ partially blocked the channel responsible for the terbutaline-stimulated Na + absorption at the Na + entry pathway across the apical membrane of the epithelium, but did not diminish the terbutaline-stimulated transcellular Na + absorption. By measuring the capacity of the Na +,K + -pump activity, we determined that the rate-limiting step of the terbutaline-stimulated transcellular Na + absorption was the extrusion step across the basolateral membrane by the Na +,K + -pump. The other Ca 2+ channel blockers, verapamil and nifedipine, had effects identical to those of Ni 2+. Based upon these observations, we conclude that, in the β-agonist-stimulated fetal rat alveolar type II epithelium, Ca 2+ channel blockers diminish amiloride-sensitive channels, but do not affect transcellular Na + absorption, since under the β-agonist-stimulated condition the Na +,K + -pump is the rate-limitng step in Na + transport.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006295202008808; http://dx.doi.org/10.1016/s0006-2952(02)00880-8; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0037091056&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/11996897; http://linkinghub.elsevier.com/retrieve/pii/S0006295202008808; http://api.elsevier.com/content/article/PII:S0006295202008808?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:S0006295202008808?httpAccept=text/plain; https://linkinghub.elsevier.com/retrieve/pii/S0006295202008808; http://dx.doi.org/10.1016/s0006-2952%2802%2900880-8; https://dx.doi.org/10.1016/s0006-2952%2802%2900880-8
Elsevier BV
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