Affordable Access

Action of cortisol on sodium transport in canine erythrocytes.

Authors
  • Streeten, D H
  • Moses, A M
Type
Published Article
Journal
The Journal of general physiology
Publication Date
Aug 01, 1968
Volume
52
Issue
2
Pages
346–362
Identifiers
PMID: 4233676
Source
Medline
License
Unknown

Abstract

Incubation of blood from deoxycorticosterone-treated, adrenalectomized dogs with glucose, (22)NaCl, and cortisol, added in vitro, revealed log dose-related acceleration of sodium influx, of glucose utilization, and of lactate formation by cortisol in concentrations between 150 and 1000 microg/liter. Addition of 2-deoxyglucose, or preincubation of the blood until blood glucose concentration had fallen below 2.0 mg per 100 ml, reduced or abolished the acceleratory action of added cortisol on sodium influx but had no effect on sodium influx in the absence of added cortisol. Cortisol did not change the ATP or ATPase content of erythrocytes, or the metabolism of glucose via the pentose phosphate pathway, or the rate of efflux of (22)Na from the erythrocytes. The acceleratory actions of cortisol on sodium, influx, glucose utilization, and lactate formation were significantly correlated. Cortisol (1000 microg/liter) enhanced sodium influx by approximately 8.7 mmole per liter erythrocytes per hour for each 1 mmole cortisol-induced increment in ATP production. It is concluded that sodium influx in canine erythrocytes comprises a passive component, unchanged by cellular metabolism, and a second component which is accelerated and inhibited in proportion to prevailing plasma concentrations of cortisol and aldosterone, and which (for cortisol) depends upon accelerated ATP production via glycolysis. These steroid actions probably result from effects on enzyme activity rather than on new enzyme induction.

Report this publication

Statistics

Seen <100 times