Sodium nitroprusside relaxes goat coronary artery through activation of calcium-dependent K+ channels.

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dc.contributor.authorDeka, Dilip Ken_US
dc.contributor.authorRavi Prakash, Vellankien_US
dc.contributor.authorMishra, Santosh Ken_US
dc.date.accessioned2009-05-28T13:11:22Z
dc.date.available2009-05-28T13:11:22Z
dc.date.issued2005-04-07en_US
dc.description.abstractIn the present investigation we have examined the hypothesis that calcium-dependent K+ channels (K(Ca)) are involved in the sodium nitroprusside (SNP)-induced vasodilatation of goat coronary artery. SNP (10(-9)-3 x 10(-6) M), added cumulatively, relaxed K+ (30 mM)-contracted coronary artery ring segments in a concentration-dependent manner with an EC50 of 1.32 x 10(-7) M (95% CL, 0.93-1.86 x 10(-7) M; n = 21). K(Ca) blocker, tetraethyl ammonium (1 mM) caused a rightward shift in the concentration-response curve of SNP with a corresponding increase in EC50 (1.62 x 10(-6) M; 95% CL, 0.44-6.02 x 10(-6) M, n = 4) of nitro vasodilator. Lowering of extra cellular Ca2+ in the physiological saline solution to 1/4 of normal selectively attenuated the vasorelaxant response of SNP, thereby causing an increase in its EC50 (2.4 x 10(-6) M; 95% CL, 1.23-4.68 x 10(-6) M, n = 4). Exposure of the tissues to high K+ (80 mM) solution, a protocol adopted to reduce the K+ gradient across the cell membrane, markedly inhibited the coronary artery relaxations induced by SNP (EC50, 2.54 x 10(-6) M; 95% CL, 1.31-4.91 x 10(-6) M, n = 4), when compared with tissues contracted with low K+ (30 mM) solution (EC50 7.9 x 10(-8); 95% CL, 4.4 x 10(-8)-1.44 x 10(-7) M, n = 6). The results suggested that a major component of SNP-induced relaxation of goat coronary artery was mediated by K(Ca) channels.en_US
dc.description.affiliationIndian Veterinary Research Institute, Izatnagar, Bareilly, India. drdilipdeka@rediffmail.comen_US
dc.identifier.citationDeka DK, Ravi Prakash V, Mishra SK. Sodium nitroprusside relaxes goat coronary artery through activation of calcium-dependent K+ channels. Indian Journal of Experimental Biology. 2005 Apr; 43(4): 324-9en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/59079
dc.language.isoengen_US
dc.source.urihttps://www.niscair.res.in/ScienceCommunication/ResearchJournals/rejour/ijeb/ijeb0.aspen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBarium Compounds --pharmacologyen_US
dc.subject.meshCalcium --metabolismen_US
dc.subject.meshChlorides --pharmacologyen_US
dc.subject.meshCoronary Vessels --drug effectsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshGoatsen_US
dc.subject.meshMethylene Blue --pharmacologyen_US
dc.subject.meshNitric Oxide Donors --pharmacologyen_US
dc.subject.meshNitroprusside --pharmacologyen_US
dc.subject.meshPotassium Channel Blockers --pharmacologyen_US
dc.subject.meshPotassium Channels, Calcium-Activated --metabolismen_US
dc.subject.meshPotassium Chloride --pharmacologyen_US
dc.subject.meshVasodilation --drug effectsen_US
dc.titleSodium nitroprusside relaxes goat coronary artery through activation of calcium-dependent K+ channels.en_US
dc.typeIn Vitroen_US
dc.typeJournal Articleen_US
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