ArticleAlcoholism, clinical and experimental research2013
Role of rostral ventrolateral medullary ERK/JNK/p38 MAPK signaling in the pressor effects of ethanol and its oxidative product acetaldehyde.
Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Acetic Acid: An Underestimated Metabolite in Ethanol-Induced Changes in Regulating Cardiovascular Function.Antioxidants (Basel, Switzerland) · 2024Review
- Long-Term Alcohol-Activated c-Jun N-terminal Kinase Isoform 2 Preserves Cardiac Function but Drives CaCells · 2023Article
- Stress-driven cardiac calcium mishandling via a kinase-to-kinase crosstalk.Pflugers Archiv : European journal of physiology · 2021Review
- Causal roles of stress kinase JNK2 in DNA methylation and binge alcohol withdrawal-evoked behavioral deficits.Pharmacological research · 2021Article
- Role of Alcohol Oxidative Metabolism in Its Cardiovascular and Autonomic Effects.Advances in experimental medicine and biology · 2019Review
- Effects of ethanol and ethanol metabolites on intrinsic function of mesenteric resistance arteries.PloS one · 2019Article
- Role of neuronal nitric oxide synthase (nNOS) at medulla in tachycardia induced by repeated administration of ethanol in conscious rats.Journal of biomedical science · 2018Article
- Salidroside protects against foam cell formation and apoptosis, possibly via the MAPK and AKT signaling pathways.Lipids in health and disease · 2017Article
- A natural small molecule, catechol, induces c-Myc degradation by directly targeting ERK2 in lung cancer.Oncotarget · 2016Article
- Ser/thr phosphatases tonically attenuate the ERK-dependent pressor effect of ethanol in the rostral ventrolateral medulla in normotensive rats.Brain research · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe tested the hypothesis that alterations of the phosphorylation/dephosphorylation profile of mitogen-activated protein kinases (MAPKs) in the rostral ventrolateral medulla (RVLM) underlie the pressor response elicited by ethanol (EtOH) microinjection into the RVLM of spontaneously hypertensive rats (SHRs). The studies were extended to determine whether acetaldehyde (ACA), the primary oxidative product of EtOH, replicates the molecular effects of EtOH within the RVLM and the consequent pressor response.
methodsEffects of EtOH or ACA on blood pressure (BP) were evaluated in the absence or presence of selective JNK (SP600125), ERK (PD98059), p38 (SB203580), or ser/thr phosphatases (okadaic acid [OKA]) inhibitor.
resultsIntra-RVLM EtOH (10 μg/rat) or ACA (2 μg/rat) caused a similar ERK2-dependent pressor response because EtOH or ACA-evoked increases in BP and in RVLM p-ERK2 level were abolished after pharmacologic inhibition of ERK phosphorylation. SP600125 abrogated the pressor action of EtOH, but not ACA, thus implicating JNK in EtOH action on BP. Despite EtOH enhancement of p38 phosphorylation, pharmacological studies argued against a causal role for this kinase in EtOH-evoked pressor response. RVLM phosphatase catalytic activity was not influenced by EtOH or ACA. Interestingly, pharmacologic phosphatase inhibition (OKA), which increased RVLM p-ERK2 and BP, abrogated the pressor effect of subsequently administered EtOH or ACA.
conclusionsEnhancement of RVLM ERK2 phosphorylation constitutes a major molecular mechanism for the pressor response elicited by intra-RVLM EtOH or its metabolite, ACA, in conscious SHRs. Further, RVLM kinases dephosphorylation does not contribute to intra-RVLM EtOH- or ACA-evoked pressor response.
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