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Chronic Alcohol Intake Induces Reversible Disturbances on Cellular Na + Metabolism in Humans: Its Relationship with Changes in Blood Pressure
Author(s) -
Coca Antonio,
Aguilera Maria T.,
Sierra Alejandro,
Sánchez Miguel,
Picado Maria J.,
Lluch Maria M.,
UrbanoMárquez Alvaro
Publication year - 1992
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1992.tb00667.x
Subject(s) - cotransporter , alcohol , blood pressure , medicine , endocrinology , stimulation , chemistry , ethanol , homeostasis , metabolism , red blood cell , sodium , biochemistry , organic chemistry
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 (V max ) and apparent dissociation constant for internal Na + (K Na ) of the Na + ‐K + pump and the Na + ‐Li + countertransport were significantly higher in alcohol consumers. A positive correlation between daily alcohol intake and V max of both transport systems ( p < 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.