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Angiotensin II type 1 receptor 1166A/C polymorphism in association with blood pressure response to exogenous angiotensin II

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dc.contributor.authorLim, Hyeong-Seok-
dc.contributor.authorCho, Joo-Youn-
dc.contributor.authorOh, Dal-Seok-
dc.contributor.authorChung, Jae-Yong-
dc.contributor.authorHong, Kyoung-Sup-
dc.contributor.authorBae, Kyun-Seop-
dc.contributor.authorYu, Kyung-Sang-
dc.contributor.authorLee, Kyung-Hoon-
dc.contributor.authorJang, In-Jin-
dc.contributor.authorShin, Sang-Goo-
dc.date.accessioned2009-12-30-
dc.date.available2009-12-30-
dc.date.issued2006-12-06-
dc.identifier.citationEur J Clin Pharmacol. 2007 Jan;63(1):17-26. Epub 2006 Dec 5.en
dc.identifier.issn0031-6970 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17146658-
dc.identifier.urihttps://hdl.handle.net/10371/23384-
dc.description.abstractBACKGROUND: The angiotensin II type 1 receptor (AT1R) 1166A/C polymorphism is reported to be implicated in cardiovascular diseases. The association between the 1166A/C polymorphism and diastolic blood pressure (DBP) changes in response to exogenous angiotensin II and valsartan was evaluated by pharmacokinetic and pharmacodynamic modeling. METHODS: Thirteen normotensive, healthy adults (six with the 1166A/A polymorphism and seven with 1166A/C) were enrolled in this clinical study. Angiotensin II was infused continuously over a 2-min period at four different rates (from 5 ng/kg/min and increased by 5 ng/kg/min) at 0 (before valsartan dosing), 2, 4, 8, 12, and 24 h after a single oral dose of valsartan (40 mg). BP was measured serially before and at the end of each rate of angiotensin II infusion. Plasma concentration-time profiles of valsartan were established over a 24-h period. We analyzed data using NONMEM and studied the relationship between the AT1R 1166A/C genotypes and BP responses. RESULTS: Plasma valsartan concentrations and DBP data best fitted into a two-compartment linear model and E(max) model (E(max) with baseline for angiotensin II and inhibitory E(max) for valsartan), respectively. The ED50 for angiotensin II in the subjects with 1166A/C [95% confidence interval (CI): 4.30 approximately 14.02 ng/kg/min] was significantly lower than in those with 1166A/A (95% CI: 14.23 approximately 28.77 ng/kg/min), while the E(max) for angiotensin II and EC50 for valsartan was similar in both genotype groups. CONCLUSIONS: These results suggest that exogenous human angiotensin II increases the BP more potently in subjects with 1166A/C than in those with 1166A/A.en
dc.language.isoenen
dc.publisherSpringer Verlagen
dc.subjectAdulten
dc.subjectAngiotensin II/*pharmacologyen
dc.subjectAngiotensin II Type 1 Receptor Blockers/pharmacologyen
dc.subjectFemaleen
dc.subjectGene Frequencyen
dc.subjectGenotypeen
dc.subjectHumansen
dc.subjectMaleen
dc.subjectReceptor, Angiotensin, Type 1/agonists/*geneticsen
dc.subjectRenin-Angiotensin System/physiologyen
dc.subjectTetrazoles/pharmacologyen
dc.subjectValine/analogs & derivatives/pharmacologyen
dc.subjectBlood Pressure-
dc.subjectPolymorphism, Single Nucleotide-
dc.titleAngiotensin II type 1 receptor 1166A/C polymorphism in association with blood pressure response to exogenous angiotensin IIen
dc.typeArticleen
dc.contributor.AlternativeAuthor임형석-
dc.contributor.AlternativeAuthor조주연-
dc.contributor.AlternativeAuthor오달석-
dc.contributor.AlternativeAuthor정재용-
dc.contributor.AlternativeAuthor홍경섭-
dc.contributor.AlternativeAuthor배균섭-
dc.contributor.AlternativeAuthor유경상-
dc.contributor.AlternativeAuthor이경훈-
dc.contributor.AlternativeAuthor장인진-
dc.contributor.AlternativeAuthor신상구-
dc.identifier.doi10.1007/s00228-006-0228-6-
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