Renin-aldosterone axis in ethanol intoxication

Nieminen, Markku M.; Fyhrquist, Frej; Linkola, Jaakko; Tikkanen, Ilkka; Tontti, K

doi:10.1016/0091-3057(81)90047-2

Cited by 17 publications

(8 citation statements)

References 12 publications

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“…After acute ethanol administration, the precursor to all steroid hormones, pregnenolone, was decreased in macaque monkeys (Porcu et al 2006) and increased in humans who were social drinkers (Pierucci-Lagha et al 2006). Likewise, following acute ethanol in cynomolgus monkeys or humans, the neuroactive steroid precursors progesterone and DOC, as well as the neuroactive metabolite 3α,5α-pregnanolone and the mineralocorticoid aldosterone are either not increased or are decreased (Porcu et al, 2006; 2010; Pierucci-Lagha et al 2006; Nieminen et al 1981). Lastly, ethanol challenge did not increase the neurosteroid DHEA in human males (Pierucci-Lagha et al 2006).…”

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confidence: 99%

Adrenal steroid hormones and ethanol self-administration in male rhesus macaques

2014

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Rationale Hypothalamic-pituitary-adrenal (HPA) axis hormones have neuroactive metabolites with receptor activity similar to ethanol. Objectives The present study related HPA hormones in naïve monkeys to ethanol self-administration. Methods Morning plasma adrenocorticotropic hormone (ACTH), cortisol, deoxycorticosterone (DOC), aldosterone and dehydroepiandrosterone-sulfate (DHEA-S) were measured longitudinally in male rhesus macaques (Macaca mulatta) induced to drink ethanol followed by access to ethanol (4% w/v, in water) and water 22 hours/day for 12 months. Results During ethanol access, DOC increased among non-heavy (average intake over 12 months ≤ 3.0 g/kg/day, n = 23) but not heavy drinkers (> 3.0 g/kg/day, n = 9), aldosterone was greater among heavy drinkers after 6 months. The ratio of DOC/aldosterone decreased only among heavy drinkers after 6 or12 months of ethanol self-administration. ACTH only correlated significantly with DHEA-S, the ratio of cortisol/DHEA-S and DOC after the onset of ethanol access, the former two just in heavy drinkers. Baseline hormones did not predict subsequent ethanol intake over 12 months, but baseline DOC correlated with average blood-ethanol concentrations (BEC), among all monkeys and heavy drinkers as a group. During ethanol access, aldosterone and DOC correlated and tended to correlate, respectively, with 12-month average ethanol intake. Conclusions Ethanol self-administration lowered ACTH and selectively altered its adrenocortical regulation. Mineralocorticoids may compensate for adrenocortical adaptation among heavy drinkers and balance fluid homeostasis. As DOC was uniquely predictive of future BEC) and not water intake, to the exclusion of aldosterone, GABAergic neuroactive metabolites of DOC may be risk factors for binge drinking to intoxication.

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Adrenal steroid hormones and ethanol self-administration in male rhesus macaques

2014

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“…Acute alcohol administration activates the renin-angiotensin system, although the effect is more robust after chronic alcohol intake (Collins, Brosnihan, Zuti, Messina, & Gupta, 1992; Linkola, Tikkanen, Fyhrquist, & Rusi, 1980; Nieminen, Linkola, Fyhrquist, Tikkanen, & Forslund, 1985; Puddey, Vandongen, Beilin, & Rouse, 1985; Stott et al, 1987; Wright, Morseth, Abhold, & Harding, 1986). There is also evidence that some of the normal functions of ANG II are blunted in the presence of ethanol.…”

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confidence: 99%

“…There is also evidence that some of the normal functions of ANG II are blunted in the presence of ethanol. For example, at moderate blood ethanol concentrations, the usual relation between plasma ANG II and aldosterone secretion appears to be broken (Collins et al, 1992; Nieminen et al, 1985).…”

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

Fitts¹,

Hoon²

1993

Behavioral Neuroscience

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Sodium depletion in rats elicits a sodium appetite that results from a cerebral action of angiotensin II (ANG II) and aldosterone. Alcohol also activates the renin-angiotensin system, but the mechanism is poorly understood and not related to sodium excretion. In this study, 2.5 g/kg ip ethanol produced a 20% decline in plasma volume and plasma protein concentration in 1-2 hr and elicited salt appetite beginning in 3-4 hr. Blockade of ANG II synthesis in the brain and periphery with the angiotensin-converting enzyme inhibitor captopril eliminated the thirst and salt appetite. Peripheral captopril alone enhanced fluid intake, which indicated that alcohol elevated renin secretion. Ethanol-induced suppression of hepatic plasma protein secretion and the consequent fall in plasma colloid osmotic pressure apparently resulted in hypovolemia and renin secretion, which then produced thirst and salt appetite through an action of ANG II on the brain.

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“…Moreover, alcohol abuse may cause volume contraction and chronic alcoholic users represent a particular population at risk ( 15 ). During alcohol intake the dehydration could in part be explained by increased diuresis due to loss of vasopressin function ( 21 ). The period of time during which dehydration had been present prior to the events in our patient was not known.…”

Section: Discussionmentioning

confidence: 99%

Forty Years Abuse of Baking Soda, Rhabdomyolysis, Glomerulonephritis, Hypertension Leading to Renal Failure: A Case Report

Forslund

Koistinen

Anttinen

et al. 2008

Clinical Medicine: Case Reports

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We present a patient who had ingested sodium bicarbonate for treatment of alcoholic dyspepsia during forty years at increasing doses. During the last year he had used more than 50 grams daily. He presented with metabolic alkalosis, epileptic convulsions, subdural hematoma, hypertension and rhabdomyolysis with end stage renal failure, for which he had to be given regular intermittent hemodialysis treatment. Untreated hypertension and glomerulonephritis was probably present prior to all these acute incidents. Examination of the kidney biopsy revealed mesangial proliferative glomerulonephritis and arterial wall thickening causing nephrosclerosis together with interstitial calcinosis. The combination of all these pathologic changes might be responsible for the development of progressive chronic renal failure ending up with the need for continuous intermittent hemodialysis treatment.

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Renin-aldosterone axis in ethanol intoxication

Cited by 17 publications

References 12 publications

Adrenal steroid hormones and ethanol self-administration in male rhesus macaques

Adrenal steroid hormones and ethanol self-administration in male rhesus macaques

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

Forty Years Abuse of Baking Soda, Rhabdomyolysis, Glomerulonephritis, Hypertension Leading to Renal Failure: A Case Report

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