Effect of chronic ethanol consumption on postnatal development of renal (Na + K)‐ATPase in the rat

Abstract

Renal (Na + K)-ATPase was studied to ascertain whether it follows the pattern of adaptation of membrane-bound enzymes that are inhibited by acute ethanol exposure and develop greater activity after chronic ethanol treatment. A colony of rats was given 20 per cent (v/v) ethanol as sole drinking solution throughout gestation, lactation and following weaning. (Na + K)-ATPase and ouabain-insensitive Ca(2+)-ATPase activities were determined; regional distribution of these enzymes was assessed in renal cortex and outer medulla. Control rats drank tap water. (Na + K)-ATPase in whole homogenate of kidney increased with age in controls and ethanol-fed rats, but the latter showed higher values at every age studied. Between 15 and 60 days of age, the control group showed 2-fold increases in cortex and 5-fold in outer medulla, whereas ethanol-fed rats reached a 3-fold increase in the enzyme activity in both renal regions. Ca(2+)-ATPase showed the same time course in developing kidney of both groups. Chronic ethanol treatment of adult rats resulted in an increase of (Na + K)-ATPase activity in cortex and outer medulla, but no change in other ATPases. Since an earlier maturational development of renal (Na + K)-ATPase was displayed by ethanol-fed rats, underlying mechanisms that may account for these results are discussed.

Ethanol and Hormesis

“…Several early reports by Rodrigo and colleagues revealed that chronic ethanol consumption in growing and adult rats causes an increase in (Na + K)-ATPase activity (Novoa and Rodrigo, 1989;Rodrigo et al, 1991). Such observations were supportive of other findings (Rodrigo et al, 1993a) of a positive sodium balance associated with a similar chronic ethanol consumption activity.…”

Long-Lasting Neural Circuit Dysfunction Following Developmental Ethanol Exposure

“…Specifically, protracted ethanol toxicity during chronic exposure cumulatively impacts other body systems that support brain development. For example, chronic alcohol exposure during gestation and lactation can negatively impact kidney function [57] and decrease fetal organ mass ratios [58]. For purposes of neural circuit examination these circumstances perturb the interpretation of causality, because the source of neurotoxicity can either be attributed to the direct interaction of alcohol, or alternatively as a byproduct of metabolic and/or systemic attrition from prolonged alcohol exposure (most likely a combination of these stressors).…”

Hypouricaemia as a Marker of a Generalized Proximal Tubular Damage in Alcoholic Patients

“…In fact, it is known that alcohol misuse may result in a generalized reduction in the reabsorptive ability of the proximal tubular cells (De Marchi et al, 1993). This hypothesis is supported by studies indicating that ethanol interferes with the carrier function of these cells by decreasing the Na + -K + -ATPase activity (Parenti et al, 1991;Rodrigo et al, 1991;Rothman et al, 1992). Furthermore, it is possible that the acetaldehyde, produced after oxidation of ethanol by alcohol dehydrogenase, may inhibit the activity of several enzymes in renal tubules (Gonzalez-Calvin et al, 1983;Rothman et al, 1992).…”