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|dc.title||Negative regulation of β-adrenergic function by hydrogen sulphide in the rat hearts|
|dc.identifier.citation||Yong, Q.C., Pan, T.-T., Hu, L.-F., Bian, J.-S. (2008). Negative regulation of β-adrenergic function by hydrogen sulphide in the rat hearts. Journal of Molecular and Cellular Cardiology 44 (4) : 701-710. ScholarBank@NUS Repository. https://doi.org/10.1016/j.yjmcc.2008.01.007|
|dc.description.abstract||β-Adrenoceptor is over-stimulated during myocardial ischemia, in which hydrogen sulphide (H2S) concentration was found to be lowered. The present study attempted to investigate if H2S modulates β-adrenoceptor function and the underlying mechanism. We examined the effect of NaHS (a H2S donor) on myocyte contraction and electrically-induced (EI) intracellular calcium ([Ca2+]i) transients upon β-adrenergic stimulation in rat ventricular myocytes with a video edge tracker method and a spectrofluorometric method using fura-2/AM as a calcium indicator, respectively. We found that isoproterenol (ISO, 10- 9-10- 6 M), a β-adrenoceptor agonist, concentration-dependently increased the twitch amplitude of ventricular myocytes, which was attenuated by NaHS (10- 5-10- 3 M) in a dose-dependent manner. The amplitudes and maximal velocities (± dl/dt) of myocyte twitch and EI-[Ca2+]i transient amplitudes were enhanced by ISO, forskolin (an adenylyl cyclase activator), 8-bromoadenosine-3′,5′-cyclic monophosphate (an activator of protein kinase A) and Bay K-8644 (a selective L-type Ca2+ channel agonist). Administration of NaHS (100 μM) only significantly attenuated the effects of ISO and forskolin. Moreover, NaHS reversed ISO-induced cAMP elevation and forskolin-stimulated adenylyl cyclase activity. In addition, stimulation of β-adrenoceptor by ISO significantly decreased endogenous H2S production in rat ventricular myocytes. In conclusion, H2S may negatively modulate β-adrenoceptor function via inhibiting adenylyl cyclase activity. Impairment of this negative modulation during ischemia may induce cardiac arrhythmias. Our study may provide a novel mechanism for ischemia-induced cardiac injury. © 2008 Elsevier Inc. All rights reserved.|
|dc.description.sourcetitle||Journal of Molecular and Cellular Cardiology|
|Appears in Collections:||Staff Publications|
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