I. A. Gallardo-Ortíz, S. N. Rodríguez-Hernández, J. J. López-Guerrero, L. Del Valle-Mondragón, P. López-Sánchez, R. M. Touyz, R. Villalobos-Molina
{"title":"α 1d肾上腺素受体在血管紧张素ii诱导的高血压中血管壁肥厚的作用","authors":"I. A. Gallardo-Ortíz, S. N. Rodríguez-Hernández, J. J. López-Guerrero, L. Del Valle-Mondragón, P. López-Sánchez, R. M. Touyz, R. Villalobos-Molina","doi":"10.1111/aap.12035","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>\n \n </p><ol>\n \n \n <li>The <i>in vivo</i> effect of continuous angiotensin II (Ang II) infusion on arterial blood pressure, vascular hypertrophy and α<sub>1</sub>-adrenoceptors (α<sub>1</sub>-ARs) expression was explored.</li>\n \n \n <li>Alzet<sup>®</sup> minipumps filled with Ang II (200 ng kg<sup>−1</sup> min<sup>−1</sup>) were subcutaneously implanted in male Wistar rats (3 months-old). Groups of rats were also treated with losartan, an AT<sub>1</sub>R antagonist, or with BMY 7378, a selective α<sub>1D</sub>-AR antagonist. Blood pressure was measured by tail-cuff; after 2 or 4 weeks of treatment, vessels were isolated for functional and structural analyses.</li>\n \n \n <li>Angiotensin II increased systolic blood pressure. Phenylephrine-induced contraction in aorta was greater (40% higher) in Ang II-treated rats than in the controls, and similar effect occurred with KCl 80 m<span>m</span>. Responses in tail arteries were not significantly different among the different groups.</li>\n \n \n <li>Angiotensin II decreased α<sub>1D</sub>-ARs without modifying the other α<sub>1</sub>-ARs and induced an increase in media thickness (hypertrophy) in aorta, while no structural change occurred in tail artery. Losartan prevented and reversed hypertension and hypertrophy, while BMY 7378 prevented and reversed the aorta's hypertrophic response, without preventing or reversing hypertension. Findings indicate that Ang II-induced aortic hypertrophic response involves Ang II-AT<sub>1</sub>Rs and α<sub>1D</sub>-ARs. Angiotensin II-induced α<sub>1D</sub>-AR-mediated vascular remodeling occurs independently of hypertension.</li>\n \n \n <li>Findings identify a α<sub>1D</sub>-AR-mediated process whereby Ang II influences aortic hypertrophy independently of blood pressure elevation.</li>\n </ol>\n \n </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2016-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12035","citationCount":"17","resultStr":"{\"title\":\"Role of α1D-adrenoceptors in vascular wall hypertrophy during angiotensin II-induced hypertension\",\"authors\":\"I. A. Gallardo-Ortíz, S. N. Rodríguez-Hernández, J. J. López-Guerrero, L. Del Valle-Mondragón, P. López-Sánchez, R. M. Touyz, R. Villalobos-Molina\",\"doi\":\"10.1111/aap.12035\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <p>\\n \\n </p><ol>\\n \\n \\n <li>The <i>in vivo</i> effect of continuous angiotensin II (Ang II) infusion on arterial blood pressure, vascular hypertrophy and α<sub>1</sub>-adrenoceptors (α<sub>1</sub>-ARs) expression was explored.</li>\\n \\n \\n <li>Alzet<sup>®</sup> minipumps filled with Ang II (200 ng kg<sup>−1</sup> min<sup>−1</sup>) were subcutaneously implanted in male Wistar rats (3 months-old). Groups of rats were also treated with losartan, an AT<sub>1</sub>R antagonist, or with BMY 7378, a selective α<sub>1D</sub>-AR antagonist. Blood pressure was measured by tail-cuff; after 2 or 4 weeks of treatment, vessels were isolated for functional and structural analyses.</li>\\n \\n \\n <li>Angiotensin II increased systolic blood pressure. Phenylephrine-induced contraction in aorta was greater (40% higher) in Ang II-treated rats than in the controls, and similar effect occurred with KCl 80 m<span>m</span>. Responses in tail arteries were not significantly different among the different groups.</li>\\n \\n \\n <li>Angiotensin II decreased α<sub>1D</sub>-ARs without modifying the other α<sub>1</sub>-ARs and induced an increase in media thickness (hypertrophy) in aorta, while no structural change occurred in tail artery. Losartan prevented and reversed hypertension and hypertrophy, while BMY 7378 prevented and reversed the aorta's hypertrophic response, without preventing or reversing hypertension. Findings indicate that Ang II-induced aortic hypertrophic response involves Ang II-AT<sub>1</sub>Rs and α<sub>1D</sub>-ARs. Angiotensin II-induced α<sub>1D</sub>-AR-mediated vascular remodeling occurs independently of hypertension.</li>\\n \\n \\n <li>Findings identify a α<sub>1D</sub>-AR-mediated process whereby Ang II influences aortic hypertrophy independently of blood pressure elevation.</li>\\n </ol>\\n \\n </div>\",\"PeriodicalId\":100151,\"journal\":{\"name\":\"Autonomic and Autacoid Pharmacology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2016-05-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1111/aap.12035\",\"citationCount\":\"17\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Autonomic and Autacoid Pharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/aap.12035\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Autonomic and Autacoid Pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/aap.12035","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Role of α1D-adrenoceptors in vascular wall hypertrophy during angiotensin II-induced hypertension
The in vivo effect of continuous angiotensin II (Ang II) infusion on arterial blood pressure, vascular hypertrophy and α1-adrenoceptors (α1-ARs) expression was explored.
Alzet® minipumps filled with Ang II (200 ng kg−1 min−1) were subcutaneously implanted in male Wistar rats (3 months-old). Groups of rats were also treated with losartan, an AT1R antagonist, or with BMY 7378, a selective α1D-AR antagonist. Blood pressure was measured by tail-cuff; after 2 or 4 weeks of treatment, vessels were isolated for functional and structural analyses.
Angiotensin II increased systolic blood pressure. Phenylephrine-induced contraction in aorta was greater (40% higher) in Ang II-treated rats than in the controls, and similar effect occurred with KCl 80 mm. Responses in tail arteries were not significantly different among the different groups.
Angiotensin II decreased α1D-ARs without modifying the other α1-ARs and induced an increase in media thickness (hypertrophy) in aorta, while no structural change occurred in tail artery. Losartan prevented and reversed hypertension and hypertrophy, while BMY 7378 prevented and reversed the aorta's hypertrophic response, without preventing or reversing hypertension. Findings indicate that Ang II-induced aortic hypertrophic response involves Ang II-AT1Rs and α1D-ARs. Angiotensin II-induced α1D-AR-mediated vascular remodeling occurs independently of hypertension.
Findings identify a α1D-AR-mediated process whereby Ang II influences aortic hypertrophy independently of blood pressure elevation.
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