Journal article
Role of inwardly rectifying K+ channels in K+-induced cerebral vasodilatation in vivo
American journal of physiology. Heart and circulatory physiology, Vol.279(6), pp.H2704-H2712
12/01/2000
DOI: 10.1152/ajpheart.2000.279.6.H2704
PMID: 11087224
Abstract
We tested whether activation of inwardly rectifying K+ (Kir) channels, Na+-K+-ATPase, or nitric oxide synthase (NOS) play a role in K+-induced dilatation of the rat basilar artery in vivo. When cerebrospinal fluid [K+] was elevated from 3 to 5, 10, 15, 20, and 30 mM, a reproducible concentration-dependent vasodilator response was elicited (change in diameter = 9 ± 1, 27 ± 4, 35 ± 4, 43 ± 12, and 47 ± 16%, respectively). Responses to K+ were inhibited by ∼50% by the Kir channel inhibitor BaCl2 (30 and 100 μM). In contrast, neither ouabain (1–100 μM, a Na+-K+-ATPase inhibitor) nor N G-nitro-l-arginine (30 μM, a NOS inhibitor) had any effect on K+-induced vasodilatation. These concentrations of K+ also hyperpolarized smooth muscle in isolated segments of basilar artery, and these hyperpolarizations were virtually abolished by 30 μM BaCl2. RT-PCR experiments confirmed the presence of mRNA for Kir2.1 in the basilar artery. Thus K+-induced dilatation of the basilar artery in vivo appears to partly involve hyperpolarization mediated by Kir channel activity and possibly another mechanism that does not involve hyperpolarization, activation of Na+-K+-ATPase, or NOS.
Details
- Title: Subtitle
- Role of inwardly rectifying K+ channels in K+-induced cerebral vasodilatation in vivo
- Creators
- Sophocles Chrissobolis - Department of Pharmacology, The University of Melbourne, Parkville, Victoria 3010, Australia; andJames Ziogas - Department of Pharmacology, The University of Melbourne, Parkville, Victoria 3010, Australia; andYi Chu - Departments of Internal Medicine and Pharmacology, Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa 52242Frank M Faraci - Departments of Internal Medicine and Pharmacology, Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa 52242Christopher G Sobey - Department of Pharmacology, The University of Melbourne, Parkville, Victoria 3010, Australia; and
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.279(6), pp.H2704-H2712
- DOI
- 10.1152/ajpheart.2000.279.6.H2704
- PMID
- 11087224
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Language
- English
- Date published
- 12/01/2000
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040312902771
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