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10.1161/HYPERTENSIONAHA.115.05396 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.115.05396 C4433413!4433413 !25870196     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25870196 &cmd=llinks): Failed to open stream: HTTP request failed! 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This study was conducted to test the hypothesis that cytochrome P450 1B1-generated metabolites of testosterone, 6?-hydroxytestosterone and 16?-hydroxytestosterone, contribute to angiotensin II-induced hypertension and its pathogenesis. Angiotensin II infusion for 2 weeks increased cardiac cytochrome P450 1B1 activity and plasma levels of 6?-hydroxytestosterone, but not 16?-hydroxytestosterone, in Cyp1b1(+/+) mice without altering Cyp1b1 gene expression; these effects of angiotensin II were not observed in Cyp1b1(-/-) mice. Angiotensin II-induced increase in systolic blood pressure and associated cardiac hypertrophy, and fibrosis, measured by intracardiac accumulation of ?-smooth muscle actin, collagen, and transforming growth factor-?, and increased nicotinamide adenine dinucleotide phosphate oxidase activity and production of reactive oxygen species; these changes were minimized in Cyp1b1(-/-) or castrated Cyp1b1(+/+) mice, and restored by treatment with 6?-hydroxytestoterone. In Cyp1b1(+/+) mice, 6?-hydroxytestosterone did not alter the angiotensin II-induced increase in systolic blood pressure; the basal systolic blood pressure was also not affected by this agent in either genotype. Angiotensin II or castration did not alter cardiac, angiotensin II type 1 receptor, angiotensin-converting enzyme, Mas receptor, or androgen receptor mRNA levels in Cyp1b1(+/+) or in Cyp1b1(-/-) mice. These data suggest that the testosterone metabolite, 6?-hydroxytestosterone, contributes to angiotensin II-induced hypertension and associated cardiac pathogenesis in male mice, most probably by acting as a permissive factor. Moreover, cytochrome P450 1B1 could serve as a novel target for developing agents for treating renin-angiotensin and testosterone-dependent hypertension and associated pathogenesis in males. Twit Text FOAVip 6 -hydroxytestosterone, a cytochrome P450 1B1 metabolite of testosterone, contributes to angiotensin II-induced hypertension and its pathogenesis in male mice ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25870196 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25870196 #FOAvip English Wikipedia <ref>{{Cite pmid|25870196 }}</ref> 6?-hydroxytestosterone, a cytochrome P450 1B1 metabolite of testosterone, contributes to angiotensin II-induced hypertension and its pathogenesis in male mice #MMPMID25870196 Pingili AK ; Kara M ; Khan NS ; Estes AM ; Lin Z ; Li W ; Gonzalez FJ ; Malik KU Hypertension 2015[Jun]; 65 (6 ): 1279-87 PMID25870196 show ga Previously, we showed that Cyp1b1 gene disruption minimizes angiotensin II-induced hypertension and associated pathophysiological changes in male mice. This study was conducted to test the hypothesis that cytochrome P450 1B1-generated metabolites of testosterone, 6?-hydroxytestosterone and 16?-hydroxytestosterone, contribute to angiotensin II-induced hypertension and its pathogenesis. Angiotensin II infusion for 2 weeks increased cardiac cytochrome P450 1B1 activity and plasma levels of 6?-hydroxytestosterone, but not 16?-hydroxytestosterone, in Cyp1b1(+/+) mice without altering Cyp1b1 gene expression; these effects of angiotensin II were not observed in Cyp1b1(-/-) mice. Angiotensin II-induced increase in systolic blood pressure and associated cardiac hypertrophy, and fibrosis, measured by intracardiac accumulation of ?-smooth muscle actin, collagen, and transforming growth factor-?, and increased nicotinamide adenine dinucleotide phosphate oxidase activity and production of reactive oxygen species; these changes were minimized in Cyp1b1(-/-) or castrated Cyp1b1(+/+) mice, and restored by treatment with 6?-hydroxytestoterone. In Cyp1b1(+/+) mice, 6?-hydroxytestosterone did not alter the angiotensin II-induced increase in systolic blood pressure; the basal systolic blood pressure was also not affected by this agent in either genotype. Angiotensin II or castration did not alter cardiac, angiotensin II type 1 receptor, angiotensin-converting enzyme, Mas receptor, or androgen receptor mRNA levels in Cyp1b1(+/+) or in Cyp1b1(-/-) mice. These data suggest that the testosterone metabolite, 6?-hydroxytestosterone, contributes to angiotensin II-induced hypertension and associated cardiac pathogenesis in male mice, most probably by acting as a permissive factor. Moreover, cytochrome P450 1B1 could serve as a novel target for developing agents for treating renin-angiotensin and testosterone-dependent hypertension and associated pathogenesis in males. |Angiotensin II/*pharmacology [MESH] |Animals [MESH] |Cardiomegaly/*physiopathology [MESH] |Castration [MESH] |Cytochrome P-450 CYP1B1/*genetics [MESH] |Disease Models, Animal [MESH] |Gene Expression Regulation [MESH] |Hydroxytestosterones/metabolism/*pharmacology [MESH] |Hypertension/drug therapy/*physiopathology [MESH] |Male [MESH] |Mice [MESH] |Random Allocation [MESH] |Reactive Oxygen Species/metabolism [MESH]6?-hydroxytestosterone, a cytochrome P450 1B1 metabolite of testostero(epmc).pdf DeepDyve Pubget Overpricing