Glucocorticoid Regulation of Rat Renal Sodium Potassium Adenosine Triphosphatase
Uniformed Services University Of The Health Sciences Bethesda United States
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Sodium potassium adenosine triphosphatase NaK-ATPase is the integral plasma membrane protein which maintains the transmembrane electrochemicalNa and K gradients required for many vital physiological functions. Glucocorticoids have been shown to enhance NaK-ATPase activity in various tissues including the kidney. An objective of this work was to investigate two possible mechanisms for glucocorticoid regulation of rat renal NaK-ATPase activity 1 through an increase in filtered sodium load and 2 by increasing the number of NaK-ATPase units through an enhanced mRNA content. The experiments involved three groups of animals adrenalectomized rats, adrenalectomized corticosterone-treated rats, and sham operated control rats. The temporal responses in GFR, filtered Na-load, and NaK-ATPase activity were compared in the three groups. In adrenalectomized rats, renal cortical NaK-ATPase activity was increased by 31 p 0.05 6 h after corticosterone administration and reached a maximal increase of 41 p 0.05 by 24 h. In the medulla, the activity increased to a maximum above control of 65 p 0.05 within 6 h. GFR and filtered Na load did not change during the 24 h after corticosterone administration. After adrenalectomy, alpha and beta subunit levels decreased 48 and 52 p 0.05, respectively, below those found in control animals. Two hours after corticosterone administration in adrenalectomized rats, the alpha and beta subunit content had risen to values that were not significantly different from those in control animals. Radioactively labeled complementary DNAs were used, in hybridization studies, to determine if this increase in subunit levels was associated with a rise in the mRNA content following corticosterone administration. After adrenalectomy, a and beta subunit mRNA levels were reduced 61 and 64 p 0.05, respectively, below control sham operated.