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| Content Provider | PubMed Central |
|---|---|
| Author | Lise, Hangaard Jessen, Peter B. Kamaev, Dmitrii Christian, Aalkjaer Matchkov, Vladimir V. |
| Copyright Year | 2015 |
| Abstract | The nature of NO- and COX-independent endothelial hyperpolarization (EDH) is not fully understood but activation of small- and intermittent-conductance Ca2+-activated K+ channels (SKCa and IKCa) is important. Previous studies have suggested that the significance of IKCa depends on [Ca2+]out. Also it has been suggested that K+ is important through localized [K+]out signaling causing activation of the Na+,K+-ATPase and inward-rectifying K+ channels (Kir). Here we tested the hypothesis that the modulating effect of [Ca2+]out on the EDH-like response depends on [K+]out. We addressed this possibility using isometric myography of rat mesenteric small arteries. When [K+]out was 4.2 mM, relaxation to acetylcholine (ACh) was stronger at 2.5 mM [Ca2+]out than at 1 mM [Ca2+]out. Inhibition of IKCa with TRAM34 suppressed the relaxations but did not change the relation between the relaxations at the low and high [Ca2+]out. This [Ca2+]out-dependence disappeared at 5.9 mM [K+]out and in the presence of ouabain or BaCl2. Our results suggest that IKCa are involved in the localized [K+]out signaling which acts through the Na+,K+-ATPase and Kir channels and that the significance of this endothelium-dependent pathway is modulated by [Ca2+]out. |
| Related Links | http://dx.doi.org/10.1155/2015/758346 |
| Starting Page | 758346 |
| File Format | |
| ISSN | 23146133 |
| e-ISSN | 23146141 |
| Journal | BioMed Research International |
| Volume Number | 2015 |
| Language | English |
| Publisher | Hindawi Publishing Corporation |
| Publisher Date | 2015-01-01 |
| Access Restriction | Open |
| Rights Holder | Hindawi Publishing Corporation |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Immunology and Microbiology Medicine Biochemistry, Genetics and Molecular Biology |
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