The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.
Swelling activates chloride current and increases internal calcium in nonpigmented epithelial cells from the rabbit ciliary body.
Membrane current and [Ca]i in rabbit nonpigmented ciliary body epithelial cells (NPE cells) were monitored with combined patch-clamp and fura-2 measurements during cell swelling induced by anisosmotic conditions. In the presence of K-channel blockers, cell swelling produced an increase in membrane current, accompanied by an increase in [Ca]i. Structural changes in the cell, associated with membrane deformation, may be the cause of the increase in [Ca]i during swelling. The conductance activated by swelling was permeable to Cl: it was dependent on the Cl concentration gradient across the cell membrane, and it was blocked by the Cl-channel blockers DIDS, SITS, NPPB, and DIOA. Although swelling increased both Cl current and [Ca]i, there was no evidence that Ca was involved in the regulation of the Cl conductance. Cell swelling activated the current even when [Ca]i was strongly buffered at an elevated level (500 nM) or at a low level (approximately 0) with internal Ca-BAPTA/Cs-BAPTA mixtures. In addition, Cl conductance was unaffected when [Ca]i was increased with a Ca ionophore. There was also no evidence that cAMP participates in the regulation of the Cl conductance: swelling activation of the current occurred in the presence of cAMP inhibitor (Rp-cAMP-S) and cAMP mimic (Sp-cAMP-S). The data suggest independent involvement of Cl conductance and internal Ca in the regulation of cell volume in NPE cells.[1]References
- Swelling activates chloride current and increases internal calcium in nonpigmented epithelial cells from the rabbit ciliary body. Botchkin, L.M., Matthews, G. J. Cell. Physiol. (1995) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Use
