| http://purl.uniprot.org/citations/25377087 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25377087 | http://www.w3.org/2000/01/rdf-schema#comment | "Arterial blood O2 levels are detected by specialized sensory organs called carotid bodies. Voltage-gated Ca(2+) channels (VGCCs) are important for carotid body O2 sensing. Given that T-type VGCCs contribute to nociceptive sensation, we hypothesized that they participate in carotid body O2 sensing. The rat carotid body expresses high levels of mRNA encoding the α1H-subunit, and α1H protein is localized to glomus cells, the primary O2-sensing cells in the chemoreceptor tissue, suggesting that CaV3.2 is the major T-type VGCC isoform expressed in the carotid body. Mibefradil and TTA-A2, selective blockers of the T-type VGCC, markedly attenuated elevation of hypoxia-evoked intracellular Ca(2+) concentration, secretion of catecholamines from glomus cells, and sensory excitation of the rat carotid body. Similar results were obtained in the carotid body and glomus cells from CaV3.2 knockout (Cacna1h(-/-)) mice. Since cystathionine-γ-lyase (CSE)-derived H2S is a critical mediator of the carotid body response to hypoxia, the role of T-type VGCCs in H2S-mediated O2 sensing was examined. Like hypoxia, NaHS, a H2S donor, increased intracellular Ca(2+) concentration and augmented carotid body sensory nerve activity in wild-type mice, and these effects were markedly attenuated in Cacna1h(-/-) mice. In wild-type mice, TTA-A2 markedly attenuated glomus cell and carotid body sensory nerve responses to hypoxia, and these effects were absent in CSE knockout mice. These results demonstrate that CaV3.2 T-type VGCCs contribute to the H2S-mediated carotid body response to hypoxia."xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpcell.00141.2014"xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/author | "Kumar G.K."xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/author | "Yuan G."xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/author | "Fox A.P."xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/author | "Peng Y.J."xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/author | "Prabhakar N.R."xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/author | "Nanduri J."xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/author | "Makarenko V.V."xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/name | "Am J Physiol Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/pages | "C146-54"xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/title | "CaV3.2 T-type Ca^2⁺ channels in H(2)S-mediated hypoxic response of the carotid body."xsd:string |
| http://purl.uniprot.org/citations/25377087 | http://purl.uniprot.org/core/volume | "308"xsd:string |
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