| http://purl.uniprot.org/citations/17379640 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17379640 | http://www.w3.org/2000/01/rdf-schema#comment | "We have recently shown that the IK1 and maxi-K channels in parotid salivary gland acinar cells are encoded by the K(Ca)3.1 and K(Ca)1.1 genes, respectively, and in vivo stimulated parotid secretion is severely reduced in double-null mice. The current study tested whether submandibular acinar cell function also relies on these channels. We found that the K(+) currents in submandibular acinar cells have the biophysical and pharmacological footprints of IK1 and maxi-K channels and their molecular identities were confirmed by the loss of these currents in K(Ca)3.1- and K(Ca)1.1-null mice. Unexpectedly, the pilocarpine-stimulated in vivo fluid secretion from submandibular glands was essentially normal in double-null mice. This result and the possibility of side-effects of pilocarpine on the nervous system, led us to develop an ex vivo fluid secretion assay. Fluid secretion from the ex vivo assay was substantially (about 75%) reduced in animals with both K(+) channel genes ablated - strongly suggesting systemic complications with the in vivo assay. Additional experiments focusing on the membrane potential in isolated submandibular acinar cells revealed mechanistic details underlying fluid secretion in K(+) channel-deficient mice. The membrane potential of submandibular acinar cells from wild-type mice remained strongly hyperpolarized (-55 +/-2 mV) relative to the Cl(-) equilibrium potential (-24 mV) during muscarinic stimulation. Similar hyperpolarizations were observed in K(Ca)3.1- and K(Ca)1.1-null mice (-51 +/- 3 and -48 +/-3 mV, respectively), consistent with the normal fluid secretion produced ex vivo. In contrast, acinar cells from double K(Ca)3.1/K(Ca)1.1-null mice were only slightly hyperpolarized (-35 +/-2 mV) also consistent with the ex vivo (but not in vivo) results. Finally, we found that the modest hyperpolarization of cells from the double-null mice was maintained by the electrogenic Na(+),K(+)-ATPase."xsd:string |
| http://purl.uniprot.org/citations/17379640 | http://purl.org/dc/terms/identifier | "doi:10.1113/jphysiol.2006.127498"xsd:string |
| http://purl.uniprot.org/citations/17379640 | http://purl.uniprot.org/core/author | "Nakamoto T."xsd:string |
| http://purl.uniprot.org/citations/17379640 | http://purl.uniprot.org/core/author | "Srivastava A."xsd:string |
| http://purl.uniprot.org/citations/17379640 | http://purl.uniprot.org/core/author | "Melvin J.E."xsd:string |
| http://purl.uniprot.org/citations/17379640 | http://purl.uniprot.org/core/author | "Begenisich T."xsd:string |
| http://purl.uniprot.org/citations/17379640 | http://purl.uniprot.org/core/author | "Romanenko V.G."xsd:string |
| http://purl.uniprot.org/citations/17379640 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17379640 | http://purl.uniprot.org/core/name | "J Physiol"xsd:string |
| http://purl.uniprot.org/citations/17379640 | http://purl.uniprot.org/core/pages | "801-817"xsd:string |
| http://purl.uniprot.org/citations/17379640 | http://purl.uniprot.org/core/title | "Regulation of membrane potential and fluid secretion by Ca2+-activated K+ channels in mouse submandibular glands."xsd:string |
| http://purl.uniprot.org/citations/17379640 | http://purl.uniprot.org/core/volume | "581"xsd:string |
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