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Article: Comparison of nitroprusside and nitroglycerin in inhibition of angiotensin II and other vasoconstrictor-mediated contraction in human coronary by pass conduits

TitleComparison of nitroprusside and nitroglycerin in inhibition of angiotensin II and other vasoconstrictor-mediated contraction in human coronary by pass conduits
Authors
KeywordsNitroprusside
aAngiotensin II
Nitroglycerin
Endothelin 1
internal mammary artery
Issue Date1997
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJCP
Citation
British Journal of Clinical Pharmacology, 1997, v. 44 n. 4, p. 361-367 How to Cite?
AbstractAIMS: To compare the effect of nitroprusside (SNP) and nitroglycerin (NTG) on angiotensin II (ANGII), endothelin-1 (ET-1), and alpha1-adrenoceptor (phenylephrine, PE)-mediated contraction in internal mammary artery (IMA). METHODS: Human IMA segments (n=120) taken from 37 patients were studied. Concentration-relaxation curves for SNP and NTG were established in IMA precontracted with these vasoconstrictors. Concentration-contraction curves were also constructed in IMA rings incubated with SNP and NTG (0.1 and 1 microM) for 10 min. RESULTS: Both SNP and NTG caused full relaxation with similar EC50s except NTG was four-fold more potent than SNP in PE-induced contraction (-7.92 +/- 0.06 vs -7.32 +/- 0.2 log M, mean +/- s.e. mean, P<0.01; 95% confidence interval for the difference of the means: 0.19, 1.01 log M). Pretreatment with SNP (0.1 and 1 microM) significantly depressed the contraction by ANGII from 56.6 +/- 7.7% (of 100 mM K+-contraction) to 18.3 +/- 8.6% and 3.9 +/- 2.1% (P=0.0001). In four rings treated with SNP, the contraction to ANGII was abolished whereas NTG did not depress ANGII-mediated contraction. Pretreatment with SNP (1 microM), but not NTG, significantly depressed the magnitude of the PE-induced contraction from 4.7 +/- 1.2 to 1.7 +/- 0.4 g (P<0.05). Treatment with both SNP and NTG significantly increased the EC50 (-5.09 +/- 0.17 log M, P=0.0007 for SNP and -5.40 +/- 0.06 log M, P=0.02 for NTG). Pretreatment with SNP did not significantly change either the magnitude or the EC50 of the ET-1-induced contraction. CONCLUSIONS: SNP may be advantageous compared with NTG in preventing coronary arterial graft contraction. However, once grafts have constricted to ANGII, alpha1-adrenoceptor agonists, and ET-1, NTG may be only marginally advantageous.
Persistent Identifierhttp://hdl.handle.net/10722/49319
ISSN
2015 Impact Factor: 3.83
2015 SCImago Journal Rankings: 1.486
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHe, GWen_HK
dc.contributor.authorYang, CQen_HK
dc.date.accessioned2008-06-12T06:39:22Z-
dc.date.available2008-06-12T06:39:22Z-
dc.date.issued1997en_HK
dc.identifier.citationBritish Journal of Clinical Pharmacology, 1997, v. 44 n. 4, p. 361-367en_HK
dc.identifier.issn0306-5251en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49319-
dc.description.abstractAIMS: To compare the effect of nitroprusside (SNP) and nitroglycerin (NTG) on angiotensin II (ANGII), endothelin-1 (ET-1), and alpha1-adrenoceptor (phenylephrine, PE)-mediated contraction in internal mammary artery (IMA). METHODS: Human IMA segments (n=120) taken from 37 patients were studied. Concentration-relaxation curves for SNP and NTG were established in IMA precontracted with these vasoconstrictors. Concentration-contraction curves were also constructed in IMA rings incubated with SNP and NTG (0.1 and 1 microM) for 10 min. RESULTS: Both SNP and NTG caused full relaxation with similar EC50s except NTG was four-fold more potent than SNP in PE-induced contraction (-7.92 +/- 0.06 vs -7.32 +/- 0.2 log M, mean +/- s.e. mean, P<0.01; 95% confidence interval for the difference of the means: 0.19, 1.01 log M). Pretreatment with SNP (0.1 and 1 microM) significantly depressed the contraction by ANGII from 56.6 +/- 7.7% (of 100 mM K+-contraction) to 18.3 +/- 8.6% and 3.9 +/- 2.1% (P=0.0001). In four rings treated with SNP, the contraction to ANGII was abolished whereas NTG did not depress ANGII-mediated contraction. Pretreatment with SNP (1 microM), but not NTG, significantly depressed the magnitude of the PE-induced contraction from 4.7 +/- 1.2 to 1.7 +/- 0.4 g (P<0.05). Treatment with both SNP and NTG significantly increased the EC50 (-5.09 +/- 0.17 log M, P=0.0007 for SNP and -5.40 +/- 0.06 log M, P=0.02 for NTG). Pretreatment with SNP did not significantly change either the magnitude or the EC50 of the ET-1-induced contraction. CONCLUSIONS: SNP may be advantageous compared with NTG in preventing coronary arterial graft contraction. However, once grafts have constricted to ANGII, alpha1-adrenoceptor agonists, and ET-1, NTG may be only marginally advantageous.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/BJCPen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsBritish Journal of Clinical Pharmacology. Copyright © Blackwell Publishing Ltd.en_HK
dc.rightsThe definitive version is available at www.blackwell-synergy.comen_HK
dc.subjectNitroprussideen_HK
dc.subjectaAngiotensin IIen_HK
dc.subjectNitroglycerinen_HK
dc.subjectEndothelin 1en_HK
dc.subjectinternal mammary arteryen_HK
dc.titleComparison of nitroprusside and nitroglycerin in inhibition of angiotensin II and other vasoconstrictor-mediated contraction in human coronary by pass conduitsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0306-5251&volume=44&issue=4&spage=361&epage=367&date=1997&atitle=Comparison+of+nitroprusside+and+nitroglycerin+in+inhibition+of+angiotensin+II+and+other+vasoconstrictor-mediated+contraction+in+human+coronary+by+pass+conduitsen_HK
dc.identifier.emailHe, GW: gwhe@hkucc.hku.hken_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1046/j.1365-2125.1997.t01-2-00589.xen_HK
dc.identifier.pmid9354311en_HK
dc.identifier.pmcidPMC2042862en_HK
dc.identifier.hkuros28529-
dc.identifier.isiWOS:A1997YA90100008-

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