title: Chronic alcohol intake induces reversible disturbances on cellular Na+ metabolism in humans: its relationship with changes in blood pressure.
abstract: The effect of chronic alcohol consumption on Na(+)-K+ ATPase, Na(+)-Li+ countertransport, outward Na(+)-K(+)-Cl- cotransport system and the Na+ leak was investigated in red blood cells from 18 normotensive subjects with a daily alcohol intake of more than 150 g. The study was repeated after 3 months of alcohol withdrawal, and results were compared with a group of 20 healthy normotensive teetotalers. Maximal efflux rate (Vmax) and apparent dissociation constant for internal Na+ (KNa) of the Na(+)-K+ pump and the Na(+)-Li+ countertransport were significantly higher in alcohol consumers. A positive correlation between daily alcohol intake and Vmax of both transport systems (p less than 0.05) was observed. These values significantly decreased after alcohol withdrawal. A simultaneous stimulation of the Na(+)-K(+)-Cl- cotransport system after alcohol withdrawal was also observed. Blood pressure values were higher in alcoholics (133.7/82.3) than in abstainers (121.4/75 mmHg) and significantly decreased (128.5/76.9 mmHg) after withdrawal. A positive correlation between the stimulation of the Na(+)-K(+)-Cl- cotransport and the decrease of blood pressure after withdrawal was observed. In conclusion, chronic alcohol intake induces disturbances on red blood cell Na+ metabolism that dissipate with the cessation of drinking. Similar abnormalities also reported in humans and animals with primary hypertension have been associated in the pathogenesis of essential hypertension. Therefore, the pressor effect of chronic alcohol intake could be mediated through these changes in cellular Na+ metabolism.
authors.affiliation: Department of General Internal Medicine, Hospital Clinico, School of Medicine, University of Barcelona, Spain.
authors.forename: A
authors.initials: A
authors.lastname: Coca
authors.forename: M T
authors.initials: MT
authors.lastname: Aguilera
authors.forename: A
authors.initials: A
authors.lastname: De la Sierra
authors.forename: M
authors.initials: M
authors.lastname: Sánchez
authors.forename: M J
authors.initials: MJ
authors.lastname: Picado
authors.forename: M M
authors.initials: MM
authors.lastname: Lluch
authors.forename: A
authors.initials: A
authors.lastname: Urbano-Márquez
mesh_terms: D000293:Adolescent; D000328:Adult; D000437:Alcoholism / Q000503:physiopathology*; D017920:Antiporters; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D002352:Carrier Proteins / Q000502:physiology; D004912:Erythrocytes / Q000187:drug effects* / Q000502:physiology; D000431:Ethanol / Q000009:adverse effects; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood*; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology; D014882:Water-Electrolyte Balance / Q000187:drug effects* / Q000502:physiology
chemical_list: D017920:Antiporters; D002352:Carrier Proteins; D015222:Sodium Channels; C045885:sodium-lithium countertransporter; D000431:Ethanol; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium