Ethanol-induced changes in plasma proteins, angiotensin II, and salt appetite in rats.

Fitts, Douglas A.; Hoon, Roxane G.

doi:10.1037/0735-7044.107.2.339

Cited by 11 publications

(6 citation statements)

References 25 publications

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“…Chronic ethanol intake has been reported to decrease APA and APN activities in mouse cerebellum [22], supporting previous findings where the increased Ang II levels were found after ethanol intake [6, 23]. Moreover, time-dependent reduction of lysosomal APN activity in mouse kidney was demonstrated 14 days after 10 and 20% ethanol administration [24].…”

Section: Discussionsupporting

confidence: 76%

Ethanol Inhibitory Effect on Rat Kidney Brush Border Aminopeptidases

Vlahović¹,

Cvetković²,

Nikolić³

et al. 2007

Nephron Exp Nephrol

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Background/Aim: Confusing data have been reported about the effect of ethanol or its metabolic products on blood pressure. The pressor agent, angiotensin II (Ang II), is found to be susceptible to degradation by different enzymes known as angiotensinases. We have studied the effects of ethanol and L-NAME, an inhibitor of nitric oxide synthase, consumption on rat serum and kidney ectoenzymes: aminopeptidase N (APN) and aminopeptidase A (APA). Methods: Enzymatic activity of both enzymes was determined spectrophotometrically in serum and 10% homogenates of the rat kidney cortex using appropriate chromogenic substrates. Results: After 2 weeks of treatment with ethanol and L-NAME, blood urea and creatinine levels were significantly increased. The activities of APN (EC 3.4.11.2) and APA (EC 3.4.11.7) were reduced in serum as well as in kidney tissue during this period. L-NAME significantly attenuated activities of both enyzmes. Ethanol and L-NAME given simultaneously did not have an additional effect on the activity of investigated enzymes. Conclusion: Hypertension caused by chronic ethanol treatment as well as L-NAME administration could be associated with the reduction of APN and APA activity. Possible ethanol- and L-NAME-mediated inhibition of angiotensins degrading aminopeptidases could potentiate their effects on blood pressure.

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Section: Discussionsupporting

confidence: 76%

Ethanol Inhibitory Effect on Rat Kidney Brush Border Aminopeptidases

Vlahović¹,

Cvetković²,

Nikolić³

et al. 2007

Nephron Exp Nephrol

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“…Ethanol accumulation might be considered a key pathway. The possible mechanisms by which ethanol increases blood pressure include: (a) a direct effect on the central nervous system, by interfering with central inhibitory pathways, which control the vasomotor center or increasing sympathetic activity, 25 (b) activation of the rennin–angiotensin system by ethanol, 26 (c) aortic endothelial oxidative injury and downregulation of the nitric oxide generating system, 27 and (d) magnesium deficiency. 28 However, the actual effect of ethanol on blood pressure is unclear.…”

Section: Discussionmentioning

confidence: 99%

Effect of alcohol and aldehyde dehydrogenase gene polymorphisms on alcohol-associated hypertension: the Guangzhou Biobank Cohort Study

et al. 2013

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The effects of alcohol dehydrogenase (ADH) 2 and aldehyde dehydrogenase (ALDH) 2 genotypes on the alcohol–blood pressure association are unclear. We examined the association of ADH2 or ALDH2 genotypes with blood pressure in older Chinese men. Based on the Guangzhou Biobank Cohort Study (GBCS), 4792 men with valid ADH2, ALDH2 genotypes were included, and genotyping of rs1229984 ADH2 and rs671 ALDH2 (AA, AG/GA or GG) was performed using a Sequenom Mass-Array platform. Information on socio-demographics and lifestyle factors, including alcohol use, was obtained from a questionnaire, and blood pressure was measured. Among alcohol drinkers, systolic and diastolic blood pressure (SBP and DBP) and mean arterial pressure (MAP) were highest for men with the GG ADH2 genotype (136.6, 77.9 and 97.5 mm Hg, respectively), followed by those with the (AA/AG ADH2+GG ALDH2) genotype (133.4, 77.6 and 96.2 mm Hg, respectively) and then the (AA/AG ADH2+AA/AG ALDH2) genotype (SBP=132.6, DBP=76.6 and MAP=95.2 mm Hg) (P for trend ranged 0.025–0.035). After adjustment for potential confounders, as well as frequency or amount of alcohol use, men with the GG ADH2 genotype were more likely to have hypertension (odds ratio (OR)=1.62, 95% confidence interval 1.15–2.28) as were men with the (AA/AG ADH2+AA/AG ALDH2) genotype (OR=1.40, 95% confidence interval 1.01–1.96) compared with men with the (AA/AG ADH2+GG ALDH2) genotype). ADH2 or ALDH2 genotypes were unrelated to hypertension among those who never drink alcohol. ADH2 genotype influences blood pressure and risk of hypertension among male alcohol drinkers, suggesting that the hypertensive effect of alcohol is due to ethanol rather than acetaldehyde.

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“…Second, a recent study reported that infusion of angiotensin II (Ang II) produced an upregulation of gp91phox expression in adipose tissue, aorta and heart (Hattori et al, 2005). Alcohol consumption robustly activates the renin-angiotensin system and increases plasma concentration of Ang II (Fitts and Hoon, 1993;Wright et al, 1986). Thus, upregualted NAD(P)H oxidase during alcohol consumption may be related to increased Ang II.…”

Section: Discussionmentioning

confidence: 97%