P. Castro-Moreno, J. P. Pardo, R. Hernández-Muñoz, J. J. López-Guerrero, L. Del Valle-Mondragón, G. Pastelín-Hernández, M. Ibarra-Barajas, R. Villalobos-Molina
{"title":"卡托普利避免高血压,血浆血管紧张素II升高,但增加血管紧张素1-7和血管紧张素II诱导的SHR离体肾灌注压","authors":"P. Castro-Moreno, J. P. Pardo, R. Hernández-Muñoz, J. J. López-Guerrero, L. Del Valle-Mondragón, G. Pastelín-Hernández, M. Ibarra-Barajas, R. Villalobos-Molina","doi":"10.1111/aap.12001","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>\n \n </p><ol>\n \n <li>We investigated captopril effects, an ACE inhibitor, on hypertension development, on Ang II and Ang-(1-7) plasma concentrations, on Ang II-induced contraction in isolated kidneys, and on kidney AT1R from spontaneously hypertensive (SHR) rats.</li>\n \n <li>Five weeks-old SHR and Wistar Kyoto (WKY) rats were treated with captopril at 30 mg/kg/day, in drinking water for 2 or 14 weeks. Systolic blood pressure (SBP) was measured, and isolated kidneys were tested for perfusion pressure and AT1R expression; while Ang II and Ang-(1-7) concentrations were determined in plasma.</li>\n \n <li>Captopril did not modify SBP in WKY rats and avoided its increase as SHR aged. Plasma Ang-II concentration was ∼4-5 folds higher in SHR rats, and captopril reduced it (P < 0.05); while captopril increased Ang-(1-7) by ∼2 fold in all rat groups.</li>\n \n <li>Captopril increased Ang II-induced pressor response in kidneys of WKY and SHR rats, phenomenon not observed in kidneys stimulated with phenylephrine, a α<sub>1</sub>-adrenoceptor agonist.</li>\n \n <li>Captopril did not modify AT1R in kidney cortex and medulla among rat strains and ages.</li>\n \n <li>Data indicate that captopril increased Ang II-induced kidney perfusion pressure but not AT<sub>1</sub>R density in kidney of WKY and SHR rats, due to blockade of angiotensin II synthesis; however, ACE inhibitors may have other actions like activating signaling processes that could contribute to their diverse effects.</li>\n </ol>\n \n </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2012-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12001","citationCount":"26","resultStr":"{\"title\":\"Captopril avoids hypertension, the increase in plasma angiotensin II but increases angiotensin 1–7 and angiotensin II-induced perfusion pressure in isolated kidney in SHR\",\"authors\":\"P. Castro-Moreno, J. P. Pardo, R. Hernández-Muñoz, J. J. López-Guerrero, L. Del Valle-Mondragón, G. Pastelín-Hernández, M. Ibarra-Barajas, R. Villalobos-Molina\",\"doi\":\"10.1111/aap.12001\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <p>\\n \\n </p><ol>\\n \\n <li>We investigated captopril effects, an ACE inhibitor, on hypertension development, on Ang II and Ang-(1-7) plasma concentrations, on Ang II-induced contraction in isolated kidneys, and on kidney AT1R from spontaneously hypertensive (SHR) rats.</li>\\n \\n <li>Five weeks-old SHR and Wistar Kyoto (WKY) rats were treated with captopril at 30 mg/kg/day, in drinking water for 2 or 14 weeks. Systolic blood pressure (SBP) was measured, and isolated kidneys were tested for perfusion pressure and AT1R expression; while Ang II and Ang-(1-7) concentrations were determined in plasma.</li>\\n \\n <li>Captopril did not modify SBP in WKY rats and avoided its increase as SHR aged. Plasma Ang-II concentration was ∼4-5 folds higher in SHR rats, and captopril reduced it (P < 0.05); while captopril increased Ang-(1-7) by ∼2 fold in all rat groups.</li>\\n \\n <li>Captopril increased Ang II-induced pressor response in kidneys of WKY and SHR rats, phenomenon not observed in kidneys stimulated with phenylephrine, a α<sub>1</sub>-adrenoceptor agonist.</li>\\n \\n <li>Captopril did not modify AT1R in kidney cortex and medulla among rat strains and ages.</li>\\n \\n <li>Data indicate that captopril increased Ang II-induced kidney perfusion pressure but not AT<sub>1</sub>R density in kidney of WKY and SHR rats, due to blockade of angiotensin II synthesis; however, ACE inhibitors may have other actions like activating signaling processes that could contribute to their diverse effects.</li>\\n </ol>\\n \\n </div>\",\"PeriodicalId\":100151,\"journal\":{\"name\":\"Autonomic and Autacoid Pharmacology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2012-09-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1111/aap.12001\",\"citationCount\":\"26\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Autonomic and Autacoid Pharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/aap.12001\",\"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.12001","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Captopril avoids hypertension, the increase in plasma angiotensin II but increases angiotensin 1–7 and angiotensin II-induced perfusion pressure in isolated kidney in SHR
We investigated captopril effects, an ACE inhibitor, on hypertension development, on Ang II and Ang-(1-7) plasma concentrations, on Ang II-induced contraction in isolated kidneys, and on kidney AT1R from spontaneously hypertensive (SHR) rats.
Five weeks-old SHR and Wistar Kyoto (WKY) rats were treated with captopril at 30 mg/kg/day, in drinking water for 2 or 14 weeks. Systolic blood pressure (SBP) was measured, and isolated kidneys were tested for perfusion pressure and AT1R expression; while Ang II and Ang-(1-7) concentrations were determined in plasma.
Captopril did not modify SBP in WKY rats and avoided its increase as SHR aged. Plasma Ang-II concentration was ∼4-5 folds higher in SHR rats, and captopril reduced it (P < 0.05); while captopril increased Ang-(1-7) by ∼2 fold in all rat groups.
Captopril increased Ang II-induced pressor response in kidneys of WKY and SHR rats, phenomenon not observed in kidneys stimulated with phenylephrine, a α1-adrenoceptor agonist.
Captopril did not modify AT1R in kidney cortex and medulla among rat strains and ages.
Data indicate that captopril increased Ang II-induced kidney perfusion pressure but not AT1R density in kidney of WKY and SHR rats, due to blockade of angiotensin II synthesis; however, ACE inhibitors may have other actions like activating signaling processes that could contribute to their diverse effects.