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|dc.title||Hydrogen sulphide in the hypothalamus causes an ATP-sensitive K+channel-dependent decrease in blood pressure in freely moving rats|
|dc.identifier.citation||Dawe, G.S., Han, S.P., Bian, J.-S., Moore, P.K. (2008). Hydrogen sulphide in the hypothalamus causes an ATP-sensitive K+channel-dependent decrease in blood pressure in freely moving rats. Neuroscience 152 (1) : 169-177. ScholarBank@NUS Repository. https://doi.org/10.1016/j.neuroscience.2007.12.008|
|dc.description.abstract||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 β-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+ (KATP) channels. In the hypothalamus, KATP channel-dependent mechanisms are involved in CNS-mediated regulation of blood pressure. In this report, we investigated the hypothesis that H2S may act via KATP 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 μM 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 μM gliclazide dose-dependently blocked the effect of 200 μM 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 μM 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 KATP channel-dependent mechanism and mimicked by endogenous H2S. © 2008 IBRO.|
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