Ethanol consumption alters the expression and reactivity of adrenomedullin in the rat mesenteric arterial bed.

doi:10.1093/alcalc/agr141

Paper

Ethanol consumption alters the expression and reactivity of adrenomedullin in the rat mesenteric arterial bed.

Published 2012 · Juliana T Rocha, U. V. Hipólito, A. Martins‐Oliveira

Alcohol and alcoholism

Q2 SJR score

12

Citations

1

Influential Citations

Full textSemantic Scholar

Abstract

AIMS Adrenomedullin (AM) is a peptide that displays cardiovascular protective activity. We investigated the effects of chronic ethanol consumption on arterial blood pressure, vascular reactivity to AM and the expression of AM system components in the rat mesenteric arterial bed (MAB). METHODS Male Wistar rats were treated with ethanol (20% vol/vol) for 6 weeks. Systolic, diastolic and mean arterial blood pressure were monitored in conscious rats. Vascular reactivity experiments were performed on isolated rat MAB. Matrix metalloproteinase-2 (MMP-2) levels were determined by gelatin zymography. Nitrite and nitrate generation were measured by chemiluminescence. Protein and mRNA levels of pre-pro-AM, CRLR (calcitonin receptor-like receptor) and RAMP1, 2 and 3 (receptor activity-modifying proteins) were assessed by western blot and quantitative real-time polymerase chain reaction, respectively. RESULTS Ethanol consumption induced hypertension and decreased the relaxation induced by AM and acetylcholine in endothelium-intact rat MAB. Phenylephrine-induced contraction was increased in endothelium-intact MAB from ethanol-treated rats. Ethanol consumption did not alter basal levels of nitrate and nitrite, nor did it affect the expression of MMP-2 or the net MMP activity in the rat MAB. Ethanol consumption increased mRNA levels of pre-pro-AM and protein levels of AM in the rat MAB. Finally, no differences in protein levels or mRNA of CRLR and RAMP1, 2 and 3 were observed after treatment with ethanol. CONCLUSION Our study demonstrates that ethanol consumption increases blood pressure and the expression of AM in the vasculature and reduces the relaxation induced by this peptide in the rat MAB.

Non-RCT

Animal Study

Study Snapshot

Ethanol consumption increases blood pressure and adrenomedullin expression in the rat mesenteric arterial bed, but reduces the relaxation induced by this peptide in the rat mesenteric arterial bed.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

Sign up to use Study Snapshot

Consensus is limited without an account. Create an account or sign in to get more searches and use the Study Snapshot.

Create an account

Paper

Ethanol consumption alters the expression and reactivity of adrenomedullin in the rat mesenteric arterial bed.

Sign up to use Study Snapshot

References

Spironolactone and hydrochlorothiazide exert antioxidant effects and reduce vascular matrix metalloproteinase‐2 activity and expression in a model of renovascular hypertension

Spironolactone and hydrochlorothiazide both reduce vascular MMP-2 activity and expression, potentially improving vascular health in renovascular hypertension.

Ethanol-Induced Expression of ET-1 and ET-BR in Liver Sinusoidal Endothelial Cells and Human Endothelial Cells Involves Hypoxia-Inducible Factor-1α and MicroRNA-1991

Ethanol-induced expression of ET-1 and ET-BR in liver cells involves HIF-1 and microRNA-1991, potentially affecting microcirculatory tone and inflammation.

Ethanol consumption increases blood pressure and alters the responsiveness of the mesenteric vasculature in rats

Chronic ethanol consumption increases blood pressure and alters the reactivity of the mesenteric bed in rats, with increased vascular response to phenylephrine maintained by increased release of vasoconstrictor prostanoids and reduced endothelial NO.

Chronic alcohol-induced oxidative endothelial injury relates to angiotensin II levels in the rat

Chronic ethanol ingestion leads to elevated angiotensin II levels, oxidative endothelial injury, depletion of endothelial NO generating system, and impaired vascular relaxation in rats.

Effect of ethanol consumption on blood pressure and rat mesenteric arterial bed, aorta and carotid responsiveness

Chronic ethanol consumption increases blood pressure and alters vascular reactivity, with effects varying depending on the agonist and blood vessel studied.

Citations

Dysregulated mitogen-activated protein kinase and matrix metalloproteinase in ethanol-induced cavernosal dysfunction.

Ethanol consumption down-regulates both MAPK and MMP pathways in rat cavernosal smooth muscle, while increasing circulating levels of MMP-9, with SAPK/JNK playing a role in ethanol-induced cavernosal dysfunction.

Electrophysiological indices of the violence inhibition mechanism and their associations with physical agression, callous-unemotional traits, and dietary omega-3

Omega-3 dietary intake may benefit physical aggression and distress-induced motor extinction, but not callous-unemotional traits/face processing.

MMP-2 and MMP-9 Activities and TIMP-1 and TIMP-2 Expression in the Prostatic Tissue of Two Ethanol-Preferring Rat Models

Chronic ethanol intake impairs prostate extracellular matrix turnover through downregulation of MMPs, potentially contributing to prostatic diseases and negatively impacting fertility.

Vascular oxidative stress: a key factor in the development of hypertension associated with ethanol consumption.

Chronic ethanol consumption leads to hypertension by increasing vascular oxidative stress and endothelial dysfunction, with reactive oxygen species (ROS) playing a key role in this process.

Pharmacological characterization of the relaxant effect induced by adrenomedullin in rat cavernosal smooth muscle

Adrenomedullin relaxes rat cavernosal smooth muscle by increasing nitrate levels and 6-keto-PGF1, which may contribute to its anti-inflammatory properties.

Hypertension and chronic ethanol consumption: What do we know after a century of study?

Chronic ethanol consumption is linked to increased blood pressure, but the exact mechanisms underlying this relationship remain elusive.

Acute ethanol intake induces mitogen-activated protein kinase activation, platelet-derived growth factor receptor phosphorylation, and oxidative stress in resistance arteries

Acute ethanol intake induces reactive oxygen species generation, PDGF-R phosphorylation, and MAPK activation through AT(1)-independent mechanisms in resistance arteries, potentially contributing to ethanol's vascular pathobiology.