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Research ArticleArticle

Ethanol Counteraction of I1-Imidazoline but NotAlpha-2 Adrenergic Receptor-Mediated Reduction in Vascular Resistance in Conscious Spontaneously Hypertensive Rats

Mahmoud M. El-Mas and Abdel A. Abdel-Rahman
Journal of Pharmacology and Experimental Therapeutics February 1999, 288 (2) 455-462;
Mahmoud M. El-Mas
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Abdel A. Abdel-Rahman
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Abstract

Our recent findings have shown that ethanol selectively counteracts decreases in blood pressure (BP) evoked via activation of central I1-imidazoline receptors but not alpha-2 adrenoceptors in conscious spontaneously hypertensive rats (SHRs). This study investigated the role of sympathetic activity, cardiac output and total peripheral resistance (TPR) in the differential effect of ethanol on centrally mediated hypotension. Changes in plasma norepinephrine (NE), as index of sympathetic activity, BP, heart rate, cardiac index, stroke volume, and TPR elicited by rilmenidine or α-methylnorepinephrine (selective I1 andalpha-2 receptor agonists, respectively) and subsequent ethanol (0.5 or 1 g/kg) or saline, were evaluated in conscious SHRs. Intracisternal rilmenidine (25 μg) or α-methylnorepinephrine (α-MNE; 4 μg) elicited similar decreases in BP, TPR, and plasma NE, but cardiac index was not changed. Ethanol (0.5 g/kg i.v.) had no effect on hemodynamic responses to rilmenidine or α-MNE. The higher dose (1 g/kg i.v.) of ethanol counteracted the hypotensive response to rilmenidine and significantly (P < .05) elevated TPR and plasma NE. In contrast, ethanol (1 g/kg) had no effect on the hypotensive responses to α-MNE but significantly (P < .05) elevated plasma NE. However, this increase in NE was approximately one third of the increase evoked by ethanol when given after rilmenidine. These findings suggest that the selective counteraction by ethanol of the hypotension evoked via activation of central I1 but not alpha-2 receptors may relate, at least in part, to its greater ability to reverse the sympathoinhibition and the associated decrease in vascular resistance mediated by I1 receptors.

Footnotes

  • Send reprint requests to: Abdel A. Abdel-Rahman, Ph.D., Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858. E-mail:rahman{at}brody.med.ecu.edu

  • ↵1 This work was supported by Grant AA07839 from the National Institute on Alcohol Abuse and Alcoholism.

  • Abbreviations:
    SHRs
    spontaneously hypertensive rats
    BP
    blood pressure
    MAP
    mean arterial pressure
    HR
    heart rate
    CO
    cardiac output
    CI
    cardiac index
    SV
    stroke volume
    RVLM
    rostral ventrolateral medulla
    NTS
    nucleus tractus solitarius
    TPR
    total peripheral resistance
    i.c.
    intracisternal, NE, norepinephrine
    α-MNE
    α-methylnorepinephrine
    • Received May 15, 1998.
    • Accepted September 2, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 288 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 288, Issue 2
1 Feb 1999
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Research ArticleArticle

Ethanol Counteraction of I1-Imidazoline but NotAlpha-2 Adrenergic Receptor-Mediated Reduction in Vascular Resistance in Conscious Spontaneously Hypertensive Rats

Mahmoud M. El-Mas and Abdel A. Abdel-Rahman
Journal of Pharmacology and Experimental Therapeutics February 1, 1999, 288 (2) 455-462;

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Research ArticleArticle

Ethanol Counteraction of I1-Imidazoline but NotAlpha-2 Adrenergic Receptor-Mediated Reduction in Vascular Resistance in Conscious Spontaneously Hypertensive Rats

Mahmoud M. El-Mas and Abdel A. Abdel-Rahman
Journal of Pharmacology and Experimental Therapeutics February 1, 1999, 288 (2) 455-462;
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