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Hydrogen sulphide in the hypothalamus causes an ATP-sensitive K+ channel-dependent decrease in blood pressure in

G S Dawe¹, S P Han, J S Bian

¹Department 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

|January 19, 2008

Summary

Hydrogen sulfide (H2S) in the hypothalamus lowers blood pressure and heart rate in rats. This effect is mediated by ATP-sensitive potassium (K(ATP)) channels and can be mimicked by endogenous H2S production.

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Area of Science:

Neuroscience
Cardiovascular Physiology
Biochemistry

Background:

Hydrogen sulfide (H2S) is an endogenous signaling molecule in the brain, primarily produced by cystathionine beta-synthase (CBS).
H2S influences neuronal activity via N-methyl-D-aspartate (NMDA) receptors and cyclic adenosine 3',5'-monophosphate (cAMP).
Vasodilatory effects of H2S are linked to ATP-sensitive potassium (K(ATP)) channels in smooth muscle.

Purpose of the Study:

To investigate the role of H2S in the hypothalamus in regulating blood pressure.
To determine if H2S acts via K(ATP) channels in the hypothalamus to control blood pressure.

Main Methods:

Mean arterial blood pressure (MAP) and heart rate were monitored in freely moving rats.
Drugs were infused into the posterior hypothalamus.
Effects of H2S donor (NaHS), K(ATP) channel blocker (gliclazide), CBS activator, and CBS inhibitors were assessed.

Main Results:

Intrahypothalamic infusion of NaHS decreased MAP and heart rate in rats.
Gliclazide dose-dependently blocked the hypotensive and bradycardic effects of NaHS.
CBS activation decreased MAP, while CBS inhibition increased MAP.

Conclusions:

H2S in the hypothalamus reduces blood pressure and heart rate in rats.
This effect is mediated by K(ATP) channels.
Endogenous H2S production in the hypothalamus influences blood pressure regulation.