Developmental change in Na,K-ATPase alpha1 and beta1 expression in normal and hypothyroid rat renal cortex

Area of Science:

• Physiology
• Endocrinology
• Nephrology

Background:

• Renal Na,K-ATPase is vital for sodium reabsorption in the nephron.
• Net sodium reabsorption significantly increases in the postnatal rat kidney.
• Thyroid status affects postnatal sodium pump isoform expression in the brain.

Purpose of the Study:

• To investigate the association between developmental increases in renal sodium transport and the abundance of Na,K-ATPase alpha(1) and beta(1) subunits.
• To determine if thyroid status influences the postnatal increase in renal Na,K-ATPase expression.

Main Methods:

• Rats were made hypothyroid using a low iodine diet, propylthiouracil, and perchlorate.
• Offspring thyroid status was assessed via triiodothyronine/thyroxine RIA.
• Renal cortical membranes were analyzed from euthyroid and hypothyroid rats aged 6 to 24 days.

Main Results:

• Na,K-ATPase activity and subunit expression did not change from 6 to 15 days.
• Between 15 and 24 days, Na,K-ATPase activity increased 1.35-fold, with alpha(1) and beta(1) subunits increasing 1.7- and 2-fold, respectively.
• In hypothyroid neonates, Na,K-ATPase activity and subunit levels showed no significant age-dependent increase.

Conclusions:

• Postnatal increases in renal sodium pump activity are due to coordinate increases in alpha(1) and beta(1) subunit expression.
• This enhanced Na,K-ATPase expression in the kidney is dependent on normal thyroid status, similar to the brain.