R. N. Kazi, A. S. Munavvar, N. A. Abdullah, A. H. Khan, E. J. Johns
{"title":"Influence of high dietary sodium intake on the functional subtypes of α1-adrenoceptors in the renal cortical vasculature of Wistar–Kyoto rats","authors":"R. N. Kazi, A. S. Munavvar, N. A. Abdullah, A. H. Khan, E. J. Johns","doi":"10.1111/j.1474-8673.2009.00428.x","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p> <b>1</b> Increased renal vascular resistance is one renal functional abnormality that contributes to hypertension, and α<sub>1</sub>-adrenoceptors play a pivotal role in modulating this renal vascular resistance. This study investigates the functional contribution of α<sub>1</sub>-adrenoceptor subtypes in the renal cortical vasculature of Wistar–Kyoto rats on a normal sodium diet (WKYNNa) compared with those given saline to drink for 6 weeks (WKYHNa).</p>\n <p> <b>2</b> The renal cortical vascular responses to the adrenergic agonists noradrenaline (NA), methoxamine (ME) and phenylephrine (PE) were measured in WKYHNa and WKYNNa rats either in the absence (the control phase) or presence of chloroethylclonidine (CEC), an α<sub>1B</sub>-adrenoceptor antagonist, 5-methylurapidil (5-MeU), an α<sub>1A</sub> antagonist, or BMY7378, an α<sub>1D</sub> antagonist.</p>\n <p> <b>3</b> Results showed a greater renal cortical vascular sensitivity to NA, PE and ME in the WKYHNa compared with WKYNNa rats (<i>P </i><<i> </i>0.05). Moreover, 5-MeU and BMY7378 attenuated adrenergically induced renal cortical vasoconstriction in WKYHNa and WKYNNa rats; this response was largely blunted in CEC-treated WKYHNa rats (all <i>P </i><<i> </i>0.05) but not in CEC-treated WKYNNa rats.</p>\n <p> <b>4</b> The data suggest that irrespective of dietary sodium content, in Wistar–Kyoto rats α<sub>1A</sub>- and α<sub>1D</sub>-subtypes are the major α<sub>1</sub>-adrenoceptors in renal cortical vasculature; however, there appears to be a functional involvement of α<sub>1B</sub>-adrenoceptors in the WKYHNa rats.</p>\n </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2009-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1474-8673.2009.00428.x","citationCount":"12","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Autonomic and Autacoid Pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/j.1474-8673.2009.00428.x","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 12
Abstract
1 Increased renal vascular resistance is one renal functional abnormality that contributes to hypertension, and α1-adrenoceptors play a pivotal role in modulating this renal vascular resistance. This study investigates the functional contribution of α1-adrenoceptor subtypes in the renal cortical vasculature of Wistar–Kyoto rats on a normal sodium diet (WKYNNa) compared with those given saline to drink for 6 weeks (WKYHNa).
2 The renal cortical vascular responses to the adrenergic agonists noradrenaline (NA), methoxamine (ME) and phenylephrine (PE) were measured in WKYHNa and WKYNNa rats either in the absence (the control phase) or presence of chloroethylclonidine (CEC), an α1B-adrenoceptor antagonist, 5-methylurapidil (5-MeU), an α1A antagonist, or BMY7378, an α1D antagonist.
3 Results showed a greater renal cortical vascular sensitivity to NA, PE and ME in the WKYHNa compared with WKYNNa rats (P <0.05). Moreover, 5-MeU and BMY7378 attenuated adrenergically induced renal cortical vasoconstriction in WKYHNa and WKYNNa rats; this response was largely blunted in CEC-treated WKYHNa rats (all P <0.05) but not in CEC-treated WKYNNa rats.
4 The data suggest that irrespective of dietary sodium content, in Wistar–Kyoto rats α1A- and α1D-subtypes are the major α1-adrenoceptors in renal cortical vasculature; however, there appears to be a functional involvement of α1B-adrenoceptors in the WKYHNa rats.