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(The FASEB Journal. 2008;22:1129.5)
© 2008 FASEB
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(The FASEB Journal. 2008;22:1129.5.)
© 2008 FASEB

1129.5

Ethanol lowers blood pressure in conscious female rats via enhancing the phosphorylation of myocardial neuronal nitric oxide synthase

Mahmoud M El-Mas, Ming Fan and Abdel A Abdel-Rahman

Pharmacology, School of Medicine, East Carolina Univ, Greenville, NC

ABSTRACT

Intragastric (i.g.) ethanol lowers blood pressure (BP) in female rats via a reduction in cardiac output (CO) and stroke volume (SV). We tested the hypothesis that enhancement of myocardial nNOS and/or eNOS activity constitutes a cellular mechanism for ethanol-evoked reductions in CO and BP. We investigated the effect of inhibition of nNOS (N{omega}-propyl-L-arginine, NPLA) or eNOS [N5-(1-iminoethyl)-L-ornithine, L-NIO] on hemodynamic, biochemical (nitrate/nitrite levels, NOx), and myocardial nNOS/eNOS phosphorylation elicited by ethanol (1 g/kg i.g.) in proestrus female rats. In saline-pretreated rats, the hemodynamic effects of ethanol (reductions in BP, CO, and SV) were coupled with increases in plasma NOx and myocardial p-nNOS, but not p-eNOS, expression. nNOS inhibition by NPLA attenuated the hemodynamic effects of ethanol and associated increases in plasma NOx and cardiac p-nNOS. eNOS inhibition by L-NIO attenuated ethanol hypotension, but not concomitant CO/SV reductions. L-NIO uncovered a dramatic increase in total peripheral resistance (TPR) in response to ethanol, which appeared to have offset the reduction in CO. These findings highlight: (i) myocardial nNOS as the cellular mechanism that underlies, in part, reductions in BP and CO caused by ethanol in female rats, and (ii) vascular eNOS-NO signaling counterbalances ethanol-induced increases in TPR.

Supported by Grant R01 AA014441 from NIAAA.





This Article
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Right arrow Articles by El-Mas, M. M
Right arrow Articles by Abdel-Rahman, A. A
PubMed
Right arrow Articles by El-Mas, M. M
Right arrow Articles by Abdel-Rahman, A. A