Chronic ethanol attenuates centrally-mediated hypotension elicited via alpha-2-adrenergic, but not I1-imidazoline, receptor activation in female rats

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dc.contributor.authorEl-Mas, Mahmoud M.en_US
dc.contributor.authorAbdel-Rahman, Abdel A.en_US
dc.date.accessioned2011-02-28T19:56:11Zen_US
dc.date.accessioned2011-05-17T13:10:56Z
dc.date.available2011-02-28T19:56:11Zen_US
dc.date.available2011-05-17T13:10:56Z
dc.date.issued2009-01-16en_US
dc.description.abstractAims—This study dealt with the effect of chronic ethanol administration on hemodynamic responses elicited by α2-adrenergic (α-methyldopa) or I1-imidazoline (rilmenidine) receptor activation in telemetered female rats. Main methods—The effects of α-methyldopa or rilmenidine on blood pressure (BP), heart rate (HR) and their variability were investigated in rats that received liquid diet without or with ethanol (5% w/v) for 12 weeks. To evaluate the effect of each drug on cardiovascular autonomic control (BP and HR variability) in the absence or presence of ethanol, three time-domain indices of hemodynamic variability were measured: (i) standard deviation of mean arterial pressure (SDMAP), (ii) standard deviation of beat-to-beat intervals, and (iii) root mean square of successive differences in R-R intervals. Key findings—In liquid diet-fed control rats, i.p. rilmenidine (600 μg/kg) or α-methyldopa (100 mg/kg) reduced BP along with decreases and increases, respectively, in HR. Both drugs had no effect on HR variability but reduced BP variability (SDMAP), suggesting a reduced vasomotor sympathetic tone. Ethanol feeding attenuated reductions in BP and SDMAP evoked by α-methyldopa but not by rilmenidine. Significance—We conclude that chronic ethanol preferentially compromises α2- but not I1- receptor-mediated hypotension in female rats probably via modulation of vasomotor sympathetic activity. These findings highlight the adequacy of rilmenidine use to lower BP in hypertensive alcoholic females.en_US
dc.identifier.citationLife Sciences; 84:3-4 p. 111-118en_US
dc.identifier.doi10.1016/j.lfs.2008.11.006
dc.identifier.pmidPMC2631659en_US
dc.identifier.urihttp://hdl.handle.net/10342/3260en_US
dc.language.isoen_USen_US
dc.publisherEast Carolina Universityen_US
dc.relation.urihttp://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T99-4TY49X7-1&_user=634873&_coverDate=01%2F16%2F2009&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_acct=C000033758&_version=1&_urlVersion=0&_userid=634873&md5=e5eafa969f754c9ae4c304e07cf62421&searchtype=aen_US
dc.rightsAuthor notified of opt-out rights by Cammie Jennings.en_US
dc.subjectEthanolen_US
dc.subjectRilmenidineen_US
dc.subjectAlpha-methyldopaen_US
dc.subjectHypotensionen_US
dc.subjectFemalesen_US
dc.subjectRatsen_US
dc.titleChronic ethanol attenuates centrally-mediated hypotension elicited via alpha-2-adrenergic, but not I1-imidazoline, receptor activation in female ratsen_US
dc.typeArticleen_US
ecu.journal.issue3-4
ecu.journal.nameLife Sciences
ecu.journal.pages111-118
ecu.journal.volume84

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