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

Dawe, Gavin S.; Han, Siew Ping; Bian, Jin-Song; Moore, Philip K.

doi:10.1016/j.neuroscience.2007.12.008

Cited by 89 publications

(67 citation statements)

References 36 publications

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“…It has been shown that NaHS induces a concentration-dependent hyperpolarization and reduces input resistance of CA1 neurons and dorsal raphe neurons through the activation of K ATP channels (Reiffenstein et al, 1992). Furthermore, microinfusion of NaHS into the hypothalamus decreases arterial blood pressure in conscious rats, an effect that is blocked by K ATP channel blocker (Dawe et al, 2008). Those findings indicate that K ATP channels are importantly involved in the action of H 2 S in the central nervous system.…”

Section: Discussionmentioning

confidence: 89%

Hydrogen Sulfide in the Rostral Ventrolateral Medulla Inhibits Sympathetic Vasomotor Tone through ATP-Sensitive K⁺ Channels

Guo

Jin²,

Wang³

et al. 2011

J Pharmacol Exp Ther

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Hydrogen sulfide (H 2 S) acts as an endogenous gaseous transmitter in the central nervous system and plays important roles in regulating cardiovascular function. The rostral ventrolateral medulla (RVLM) is a putative critical central region in the control of sympathetic vasomotor tone and plays an important role in the baroreflex by integrating the inputs from a variety of visceral and somatic stimuli. In this study, we tested the hypothesis that H 2 S decreases sympathetic vasomotor tone through ATP-sensitive potassium channels (K ATP ) in the RVLM. The arterial blood pressure (ABP), heart rate (HR), and renal sympathetic nerve activity (RSNA) of anesthetized rats were recorded. Bilateral microinjections of sodium hydrosulfide (NaHS; 4, 8, and 16 mM, 50 nl), an H 2 S donor, into the RVLM decreased ABP, HR, and RSNA in a dose-dependent manner. Preinjection of glibenclamide (40 M, 50 nl), a K ATP channel blocker, abolished the sympathoinhibitory effects of NaHS (8 mM, 50 nl). Preinjection of a nitric-oxide synthase inhibitor, N -nitro-L-arginine methyl ester (200 M, 50 nl) partially inhibited the sympathoinhibitory effects of NaHS. Prior microinjection of 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-[trifluoromethyl]phenyl)pyridine-3-carboxylic acid methyl ester (Bay K8644) (1 M, 50 nl), an agonist of Ca 2ϩ channels, did not alter the effects of NaHS. Infusion of hydroxylamine (30 mM, 50 nl), a cystathionine ␤-synthase inhibitor, increased ABP, HR, and RSNA. Taken together, these findings suggest that exogenous H 2 S in the RVLM inhibits sympathetic vasomotor tone by opening K ATP channels. Nitricoxide signaling may partially be involved in the sympathoinhibitory effect of H 2 S in the RVLM.

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Section: Discussionmentioning

confidence: 89%

Hydrogen Sulfide in the Rostral Ventrolateral Medulla Inhibits Sympathetic Vasomotor Tone through ATP-Sensitive K⁺ Channels

Guo

Jin²,

Wang³

et al. 2011

J Pharmacol Exp Ther

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“…It has been shown that microinfusion of NaHS into the hypothalamus decreases arterial blood pressure by opening ATP-sensitive potassium (K ATP ) channels (9). Furthermore, we have shown that H 2 S increases the sensitivity of the carotid sinus baroreflex, an effect that is blocked by K ATP channel blocker (30,31).…”

mentioning

confidence: 68%

“…The histological identification was made to verify each microinjection site. An adenoviral suspension (1ϫ10 9 plaque forming units/ml) was injected into the bilateral RVLM within 10 min with a syringe infusion pump (KDS101, KD Scientific, Hollistion, MA). The total volume of the injection was 100 nl for each side of the RVLM.…”

Section: General Procedures and Gene Transfer Into The Rvlm In Vivomentioning

confidence: 99%

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Gene transfer of cystathionine β-synthase into RVLM increases hydrogen sulfide-mediated suppression of sympathetic outflow via K_ATP channel in normotensive rats

Duan

Guo

Liu

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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transfer of cystathionine ␤-synthase into RVLM increases hydrogen sulfide-mediated suppression of sympathetic outflow via KATP channel in normotensive rats. Am J Physiol Heart Circ Physiol 308: H603-H611, 2015. First published January 16, 2015; doi:10.1152/ajpheart.00693.2014.-Hydrogen sulfide has been shown to have a sympathoinhibitory effect in the rostral ventrolateral medulla (RVLM). The present study examined the function of cystathionine ␤-synthase (CBS)/hydrogen sulfide system in the RVLM, which plays a crucial role in the control of blood pressure and sympathetic nerve activity. Adenovirus vectors encoding CBS (Ad-CBS) or enhanced green fluorescent protein (AdEGFP) were transfected into the RVLM in normotensive rats. Identical microinjection of AdCBS into the RVLM had no effect on systolic blood pressure and heart rate (HR) in conscious rats. Acute experiments were performed at day 7 after gene transfer in anesthetized rats. Microinjection of the CBS inhibitors hydroxylamine (HA) or amino-oxyacetate into the RVLM produced an increase in the renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), and HR. There was a potentiation of the increases in RSNA, MAP, and HR because of the CBS inhibitors in AdCBS-injected rats compared with Ad-EGFP-injected rats. Pretreatment with pinacidil, a ATP-sensitive potassium (K ATP) channel activator, abolished the effects of HA in two groups. Microinjection of glibenclamide, a K ATP channel blocker, produced increases in RSNA, MAP, and HR in AdCBS-injected rats. No changes in behavior were observed in AdEGFP-injected rats. Furthermore, Western blot analysis indicated an increase in the expression of sulfonylurea receptor 2 and inward rectifier K ϩ 6.1 in AdCBS-injected rats. These results suggest that the increase in K ATP channels in the RVLM may be responsible for the greater sympathetic outflow and pressor effect of HA in AdCBS-injected rats compared with AdEGFP-injected rats.cystathionine ␤-synthase; rostral ventrolateral medulla; renal sympathetic nerve activity; gene transfer; blood pressure HYDROGEN SULFIDE (H 2 S) is an endothelium-derived hyperpolarizing factor that enhances relaxation of the peripheral vasculature (2, 28). Recent studies (9, 13, 34) have also reported its physiological functions in the central nervous system. In mammalian tissues, H 2 S is produced through degradation of L-cysteine mainly by two main enzymes: cystathionine ␤-synthase (CBS) and cystathionine ␥-lyase (15). CBS is primarily found in the brain, whereas CSE is mainly expressed in the peripheral tissues (15). CBS has been found in regions of the brain, such as the paraventricular nucleus (11) and rostral ventrolateral medulla (RVLM) (13), which are responsible for the regulation of sympathetic nerve activity and thus arterial blood pressure.However, conflicting results have also been reported regarding the role of H 2 S in regulating sympathetic nerve activity and blood pressure. Previous experiments have demonstrated that bilateral microinjection of sodium hydrosulfid...

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“…Але особливого значення дослідження його впливу на функ-ціонування організму набули лише в останні роки [3]. Біологічні ефекти H 2 S пов'язані з регуляцією серцево-судинної, імунної, ен-докринної, видільної, сенсорної та нервової систем [4][5][6][7][8]. Однак однією з найважливіших властивостей сірководню є його потужна судинорозширювальна дія [9,10].…”

Section: вступunclassified

Тне Rоle of Hydrogen Sulfide in Regulation of Circulation Blood Liver

Yanchuk¹,

Slobodianyk²

2015

Fiziol Zh

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

Cited by 89 publications

References 36 publications

Hydrogen Sulfide in the Rostral Ventrolateral Medulla Inhibits Sympathetic Vasomotor Tone through ATP-Sensitive K⁺ Channels

Hydrogen Sulfide in the Rostral Ventrolateral Medulla Inhibits Sympathetic Vasomotor Tone through ATP-Sensitive K⁺ Channels

Gene transfer of cystathionine β-synthase into RVLM increases hydrogen sulfide-mediated suppression of sympathetic outflow via K_ATP channel in normotensive rats

Тне Rоle of Hydrogen Sulfide in Regulation of Circulation Blood Liver

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

Cited by 89 publications

References 36 publications

Hydrogen Sulfide in the Rostral Ventrolateral Medulla Inhibits Sympathetic Vasomotor Tone through ATP-Sensitive K+ Channels

Hydrogen Sulfide in the Rostral Ventrolateral Medulla Inhibits Sympathetic Vasomotor Tone through ATP-Sensitive K+ Channels

Gene transfer of cystathionine β-synthase into RVLM increases hydrogen sulfide-mediated suppression of sympathetic outflow via KATP channel in normotensive rats

Тне Rоle of Hydrogen Sulfide in Regulation of Circulation Blood Liver

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Hydrogen Sulfide in the Rostral Ventrolateral Medulla Inhibits Sympathetic Vasomotor Tone through ATP-Sensitive K⁺ Channels

Hydrogen Sulfide in the Rostral Ventrolateral Medulla Inhibits Sympathetic Vasomotor Tone through ATP-Sensitive K⁺ Channels

Gene transfer of cystathionine β-synthase into RVLM increases hydrogen sulfide-mediated suppression of sympathetic outflow via K_ATP channel in normotensive rats