| http://purl.uniprot.org/citations/16141800 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16141800 | http://www.w3.org/2000/01/rdf-schema#comment | "The present study aimed to determine whether a polymorphism in CYP3A5, encoding the major CYP3A enzyme in the human kidney, is associated with blood pressure in Caucasians. A homogenous group of 115 young, white male students with normal or mildly elevated, but untreated blood pressure was included. Blood pressure was recorded by ambulatory 24-h blood pressure-monitoring and compared between individuals with high (*1/*3) and low CYP3A5 expression (*3/*3). Moreover, genotype-dependent differences in parameters associated with the renin-angiotensin-aldosterone system were evaluated. Twenty-four hour diastolic blood pressure values were not significantly different between the two groups. However, individuals with the CYP3A5*3/*3 genotype had significantly higher 24-h ambulatory systolic blood pressure values compared to subjects with the CYP3A5*1/*3 genotype (129+/-10 versus 124+/-9, P < 0.05). There was no association of CYP3A5 genotype with angiotensin II plasma concentrations, renal plasma flow, glomerular filtration rate, urinary sodium excretion and parameters determined by echocardiography, but the *3/*3 group had significantly lower serum aldosterone concentrations compared to the individuals with the *1/*3 genotype (101+/-29 versus 117+/-29 pg/ml, P < 0.05). These data, as generated with a homogenous population of young Caucasians, indicate that the CYP3A5 genotype affects blood pressure in humans possibly by genotype-dependent differences in renal, CYP3A5-mediated metabolism of cortisol and/or aldosterone. We interpret the lower serum aldosterone concentration in the genotype group with the elevated systolic blood pressure as a counter-regulatory mechanism to attenuate the increased blood pressure associated with the CYP3A5*3/*3 genotype."xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://purl.org/dc/terms/identifier | "doi:10.1097/01.fpc.0000175599.49764.98"xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://purl.uniprot.org/core/author | "Pahl A."xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://purl.uniprot.org/core/author | "Fromm M.F."xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://purl.uniprot.org/core/author | "Schmidt B.M."xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://purl.uniprot.org/core/author | "Jacobi J."xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://purl.uniprot.org/core/author | "Schmieder R.E."xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/16141800 | http://purl.uniprot.org/core/name | "Pharmacogenet Genomics"xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://purl.uniprot.org/core/pages | "737-741"xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://purl.uniprot.org/core/title | "CYP3A5 genotype is associated with elevated blood pressure."xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://purl.uniprot.org/core/volume | "15"xsd:string |
| http://purl.uniprot.org/citations/16141800 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16141800 |
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