Volume 19, Issue 4 (December 2015)                   Physiol Pharmacol 2015, 19(4): 263-273 | Back to browse issues page

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Salihi A B. Activation of Inward Rectifier Potassium Channels in High Salt Impairment of Hydrogen Sulfide-Induced Aortic Relaxation in Rats. Physiol Pharmacol. 2015; 19 (4) :263-273
URL: http://ppj.phypha.ir/article-1-1137-en.html
Abstract:   (4497 Views)

Introduction: Hydrogen sulfide (H2S) plays a key role in the regulation of vascular tone and protection of blood vessels against endothelial dysfunction. Since the mechanism of salt impairing H2S-induced vascular relaxation is not fully clear, therefore this study was designed to investigate the role of potassium (K+) channels in the vasodilatory effects of exogenous H2S in rat aortic rings. Materials and Methods: Isolated thoracic aortic rings of adult male albino rats fed 8% NaCl diet for six weeks were used for isometric tension recording using PowerLab tissue bath system. Results: The relaxation response to sodium disulfide (Na2S, an H2S donor) was reduced in aortic rings of rats that were either fed high salt (HS) or incubated in a medium containing 1,3 or 5mM/L of extra NaCl compared with control rings. Na2S-induced relaxation was lower in rings precontracted by high K+ than phenylephrine (PE, a selective α1adrenergic receptor agonist). In addition, incubation of aortic rings of HS loaded rats with inward-rectifier K+ (KIR) channels blocker individually or simultaneously with either ATP-dependent (KATP) or voltage-sensitive K+ (KV) channels blockers inhibited Na2S-induced relaxation in PE-precontracted rings; however it had no effects on rings pretreated with KATP channels blocker. In contrast, incubation of aortic rings of HS loaded rats with Ca+2 activated K+ (KCa) channels blocker individually or in combination with KIR channels blocker significantly enhanced Na2S-induced relaxation. Conclusion: These results revealed that HS partially impairs aortic relaxation caused by H2S, and that the mechanism of relaxation is mainly mediated by the stimulation of KIR channels and inhibition of KCa channels.

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