Literature DB >> 15834230

Brainstem norepinephrine neurons mediate ethanol-evoked pressor response but not baroreflex dysfunction.

Guichu Li1, Xu Wang, Abdel A Abdel-Rahman.   

Abstract

BACKGROUND: Ethanol elicits strain-dependent blood pressure and baroreflex sensitivity responses in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats; the mechanisms underlying these divergent effects are not clear. The authors tested the hypothesis that differential neuronal actions of ethanol may account for these strain-dependent responses. To this end, the authors investigated the direct effects of ethanol on norepinephrine (NE)-containing neurons in the rostral ventrolateral medulla (RVLM), which modulate sympathetic neuronal activity, and on c-Jun-expressing neurons in the nucleus tractus solitarius (NTS), whose activity is inversely correlated with baroreflex sensitivity.
METHODS: In a newly developed model system in conscious, freely moving rats, the effect of intra-RVLM or intra-NTS ethanol was investigated on neuronal NE at the microinjection site (in vivo electrochemistry), blood pressure, heart rate, spontaneous baroreflex sensitivity, and c-Jun expression in the NTS.
RESULTS: Ethanol (1, 5, or 10 microg) microinjection into the RVLM elicited dose-dependent increases in RVLM NE and blood pressure in SHRs but not in WKY rats. Ethanol had no effect on the activity of the NE-containing neurons in the NTS of either strain. However, baroreflex dysfunction elicited by intra-NTS ethanol in conscious WKY rats was associated with enhanced expression of c-Jun in the NTS.
CONCLUSIONS: (1) Ethanol activation of the NE-containing neurons in the RVLM of SHRs contributes to the centrally mediated pressor response, (2) the NE-containing neurons in the NTS are not involved in ethanol-induced baroreflex dysfunction, and (3) direct activation of the c-Jun-containing neurons in the NTS is implicated in baroreflex dysfunction elicited by ethanol in normotensive rats.

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Year:  2005        PMID: 15834230     DOI: 10.1097/01.alc.0000160083.72579.ec

Source DB:  PubMed          Journal:  Alcohol Clin Exp Res        ISSN: 0145-6008            Impact factor:   3.455


  9 in total

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2.  Enhanced hemeoxygenase activity in the rostral ventrolateral medulla mediates exaggerated hemin-evoked hypotension in the spontaneously hypertensive rat.

Authors:  Noha N Nassar; Guichu Li; Aurel L Strat; Abdel A Abdel-Rahman
Journal:  J Pharmacol Exp Ther       Date:  2011-07-18       Impact factor: 4.030

3.  Role of rostral ventrolateral medullary ERK/JNK/p38 MAPK signaling in the pressor effects of ethanol and its oxidative product acetaldehyde.

Authors:  Mahmoud M El-Mas; Ming Fan; Abdel A Abdel-Rahman
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4.  Enhanced catabolism to acetaldehyde in rostral ventrolateral medullary neurons accounts for the pressor effect of ethanol in spontaneously hypertensive rats.

Authors:  Mahmoud M El-Mas; Abdel A Abdel-Rahman
Journal:  Am J Physiol Heart Circ Physiol       Date:  2011-12-09       Impact factor: 4.733

5.  Estrogen modulation of the ethanol-evoked myocardial oxidative stress and dysfunction via DAPK3/Akt/ERK activation in male rats.

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6.  Estrogen-dependent enhancement of NO production in the nucleus tractus solitarius contributes to ethanol-induced hypotension in conscious female rats.

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7.  Forebrain and hindbrain effects of ethanol on counterregulatory responses to hypoglycemia in conscious rats.

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8.  Facilitation of central imidazoline I(1)-site/extracellular signal-regulated kinase/p38 mitogen-activated protein kinase signalling mediates the hypotensive effect of ethanol in rats with acute renal failure.

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9.  Ser/thr phosphatases tonically attenuate the ERK-dependent pressor effect of ethanol in the rostral ventrolateral medulla in normotensive rats.

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  9 in total

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