| Hydrogen sulphide in the hypothalamus causes an ATP-sensitive K+ channel-dependent decrease in blood pressure in freely moving rats. | |
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MedLine Citation:
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PMID: 18201837 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Hydrogen sulfide (H2S) is a naturally occurring gas that may act as an endogenous signaling molecule. In the brain, H2S is mainly produced by cystathionine beta-synthase (CBS) and its cellular effects have been attributed to interactions with N-methyl-D-aspartate (NMDA) receptors and cyclic adenosine 3',5'-monophosphate (cAMP). In contrast, direct vasodilator actions of H2S are most probably mediated by opening smooth muscle ATP-sensitive K+ (K(ATP)) channels. In the hypothalamus, K(ATP) channel-dependent mechanisms are involved in CNS-mediated regulation of blood pressure. In this report, we investigated the hypothesis that H2S may act via K(ATP) channels in the hypothalamus to regulate blood pressure. Mean arterial blood pressure (MAP) and heart rate were monitored in freely moving rats via a pressure transducer placed in the femoral artery. Drugs were infused via a cannula placed in the posterior hypothalamus. Infusion of 200 microM sodium hydrogen sulfide (NaHS), an H2S donor, into the hypothalamus of freely moving rats reduced MAP and heart rate. Infusion of 300 nM to 3 microM gliclazide dose-dependently blocked the effect of 200 microM NaHS. Infusion of the CBS activator, s-adenosyl-L-methionine (0.1 mM and 1 mM), likewise decreased MAP. Infusion of the CBS inhibitors aminooxyacetic acid (10 mM) and hydroxylamine (20 mM) increased MAP but did not block the effects of infusion of 200 microM NaHS. These data indicate that actions of H2S in the hypothalamus decrease blood pressure and heart rate in freely moving rats. This effect appears to be mediated by a K(ATP) channel-dependent mechanism and mimicked by endogenous H2S. |
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Authors:
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G S Dawe; S P Han; J S Bian; P K Moore |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Neuroscience Volume: 152 ISSN: 0306-4522 ISO Abbreviation: Neuroscience Publication Date: 2008 Mar |
Date Detail:
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Created Date: 2008-06-30 Completed Date: 2008-08-05 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7605074 Medline TA: Neuroscience Country: United States |
Other Details:
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Languages: eng Pagination: 169-77 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Centre for Life Sciences, 28 Medical Drive, Singapore 117456. gavindawe@nus.edu.sg |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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metabolism* Animals Blood Pressure / drug effects, physiology* Cystathionine beta-Synthase / drug effects, metabolism Enzyme Inhibitors / pharmacology Heart Rate / drug effects, physiology Hydrogen Sulfide / metabolism* Hypothalamus / drug effects, metabolism* Male Movement Potassium Channels / drug effects, metabolism* Rats Rats, Sprague-Dawley |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; 0/Potassium Channels; 56-65-5/Adenosine Triphosphate; 7783-06-4/Hydrogen Sulfide; EC 4.2.1.22/Cystathionine beta-Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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