REGULATION OF RAT RENAL ALPHA(2B)-ADRENERGIC RECEPTORS BY POTASSIUM-DEPLETION

Potassium depletion and alpha(2)-adrenergic receptor (alpha(2)-AR) ago nists produce similar physiological effects on renal function. Both st imuli increase Na-H exchange in proximal tubule cells, inhibit water t ransport in collecting tubule cells, and alter blood pressure regulati on. The purpose of this study was to determine whether potassium deple tion and renal alpha(2)-AR subtype expression were linked. Kidney memb rane proteins and RNA were harvested from anesthetized rats fed a pota ssium-deficient diet for 4-20 days (LK 4 to LK 20). Using a selective alpha(2)-AR antagonist, [H-3]MK-912, we observed that potassium deplet ion led to a dramatic increase in maximum binding (270% of control) wi thout a change in dissociation constant. Competitive binding studies i n LK 14 kidney mem branes employing chlorpromazine, prazosin, and oxym etazoline suggested that the increase in alpha(2)-ARs in response to p otassium depletion was due primarily to an increase in the B subtype o f alpha(2)-AR. Northern blot analysis demonstrated that renal alpha(2B )-AR mRNA levels increased (190% of control) after 4 or 14 days on a p otassium-deficient diet. In contrast, there was no difference in stead y-state alpha(2A)-receptor protein levels by Western blot analysis. We conclude that potassium depletion selectively increases the expressio n of the B subtype of alpha(2)-AR with no detectable effect on alpha(2 A)-AR expression.