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Inhibition of carbachol-evoked oscillatory currents by the NO donor sodium nitroprusside in guinea-pig ileal myocytes

DC Field Value Language
dc.contributor.author남택상-
dc.contributor.author안덕선-
dc.contributor.author이영호-
dc.contributor.author이홍기-
dc.contributor.author정승수-
dc.date.accessioned2017-05-04T07:32:35Z-
dc.date.available2017-05-04T07:32:35Z-
dc.date.issued2005-
dc.identifier.issn0958-0670-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/147433-
dc.description.abstractThe effect of sodium nitroprusside (SNP) on carbachol (CCh)-evoked inward cationic current (Icat) oscillations in guinea-pig ileal longitudinal myocytes was investigated using the whole-cell patch-clamp technique and permeabilized longitudinal muscle strips. SNP (10 microm) completely inhibited I(cat) oscillations evoked by 1 microm CCh. 1H-(1,2,4) Oxadiazole [4,3-a] quinoxaline-1-one (ODQ; 1 microm) almost completely prevented the inhibitory effect of SNP on Icat oscillations. 8-Bromo-guanosine 3',5'-cyclic monophosphate (8-Br-cGMP; 30 microm) in the pipette solution completely abolished Icat oscillations. However, a pipette solution containing Rp-8-Br-cGMP (30 microm) almost completely abolished the inhibitory effect of SNP on Icat oscillations. When the intracellular calcium concentration ([Ca2+]i) was held at a resting level using BAPTA (10 mm) and Ca2+ (4.6 microm) in the pipette solution, CCh (1 microm) evoked only the sustained component of Icat without any oscillations and SNP did not affect the current. A high concentration of inositol 1,4,5-trisphosphate (IP3; 30 microm) in the patch pipette solutions significantly reduced the inhibitory effect of SNP (10 microm) on Icat oscillations. SNP significantly inhibited the Ca2+ release evoked by either CCh or IP3 but not by caffeine in permeabilized preparations of longitudinal muscle strips. These results suggest that the inhibitory effects of SNP on Icat oscillations are mediated, in part, by functional modulation of the IP3 receptor, and not by the inhibition of cationic channels themselves or by muscarinic receptors in the plasma membrane. This inhibition seems to be mediated by an increased cGMP concentration in a protein kinase G-dependent manner.-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.languageEnglish-
dc.publisherWiley-Blackwell-
dc.relation.isPartOfEXPERIMENTAL PHYSIOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCaffeine/pharmacology-
dc.subject.MESHCarbachol/antagonists & inhibitors*-
dc.subject.MESHCarbachol/pharmacology-
dc.subject.MESHChelating Agents/pharmacology-
dc.subject.MESHCyclic GMP/analogs & derivatives-
dc.subject.MESHCyclic GMP/pharmacology-
dc.subject.MESHCyclic GMP-Dependent Protein Kinases/physiology-
dc.subject.MESHEgtazic Acid/analogs & derivatives-
dc.subject.MESHEgtazic Acid/pharmacology-
dc.subject.MESHGuinea Pigs-
dc.subject.MESHIleum/drug effects-
dc.subject.MESHIleum/physiology-
dc.subject.MESHIn Vitro Techniques-
dc.subject.MESHMembrane Potentials/drug effects-
dc.subject.MESHMuscarinic Agonists/pharmacology*-
dc.subject.MESHMuscle Contraction/drug effects-
dc.subject.MESHMuscle Contraction/physiology-
dc.subject.MESHMyocytes, Smooth Muscle/drug effects-
dc.subject.MESHMyocytes, Smooth Muscle/physiology*-
dc.subject.MESHNitric Oxide Donors/pharmacology*-
dc.subject.MESHNitroprusside/pharmacology*-
dc.subject.MESHOxadiazoles/pharmacology-
dc.subject.MESHPatch-Clamp Techniques-
dc.subject.MESHPhosphatidylinositol 3-Kinases/pharmacology-
dc.subject.MESHPhosphodiesterase Inhibitors/pharmacology-
dc.subject.MESHQuinoxalines/pharmacology-
dc.subject.MESHType C Phospholipases/pharmacology-
dc.titleInhibition of carbachol-evoked oscillatory currents by the NO donor sodium nitroprusside in guinea-pig ileal myocytes-
dc.typeArticle-
dc.publisher.locationEngland-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Physiology (생리학교실)-
dc.contributor.departmentDept. of Physiology (생리학교실)-
dc.contributor.departmentDept. of Physiology (생리학교실)-
dc.contributor.departmentDept. of Family Medicine (가정의학교실)-
dc.contributor.departmentDept. of Physiology (생리학교실)-
dc.contributor.googleauthorSeung-Soo Chung-
dc.contributor.googleauthorDuck-Sun Ahn-
dc.contributor.googleauthorHong-Ghi Lee-
dc.contributor.googleauthorYoung-Ho Lee-
dc.contributor.googleauthorTaick-Sang Nam-
dc.identifier.doi10.1113/expphysiol.2004.029611-
dc.contributor.localIdA01271-
dc.contributor.localIdA02223-
dc.contributor.localIdA02968-
dc.contributor.localIdA03330-
dc.contributor.localIdA03643-
dc.relation.journalcodeJ00876-
dc.identifier.eissn1469-445X-
dc.identifier.pmid15833757-
dc.subject.keyword15833757-
dc.contributor.alternativeNameNam, Taick Sang-
dc.contributor.alternativeNameAhn, Duk Sun-
dc.contributor.alternativeNameLee, Young Ho-
dc.contributor.alternativeNameLee, Hong Ki-
dc.contributor.alternativeNameChung, Seung Soo-
dc.citation.volume90-
dc.citation.number4-
dc.citation.startPage577-
dc.citation.endPage586-
dc.identifier.bibliographicCitationEXPERIMENTAL PHYSIOLOGY, Vol.90(4) : 577-586, 2005-
dc.date.modified2017-05-04-
dc.identifier.rimsid40216-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Family Medicine (가정의학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers

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