Regulation of rat renal α(2B)-adrenergic receptors by potassium depletion

Potassium depletion and α₂-adrenergic receptor (α₂-AR) agonists produce similar physiological effects on renal function. Both stimuli increase Na-H exchange in proximal tubule cells, inhibit water transport in collecting tubule cells, and alter blood pressure regulation. The purpose of this study was to determine whether potassium depletion and renal α₂-AR subtype expression were linked. Kidney membrane proteins and RNA were harvested from anesthetized rats fed a potassium-deficient diet for 4-20 days (LK 4 to LK 20). Using a selective α₂-AR antagonist, [³H]MK-912, we observed that potassium depletion led to a dramatic increase in maximum binding (270% of control) without a change in dissociation constant. Competitive binding studies in LK 14 kidney membranes employing chlorpromazine, prazosin, and oxymetazoline suggested that the increase in α₂-ARs in response to potassium depletion was due primarily to an increase in the B subtype of α₂-AR. Northern blot analysis demonstrated that renal α(2B)-AR mRNA levels increased (190% of control) after 4 or 14 days on a potassium-deficient diet. In contrast, there was no difference in steady- state α(2A)-receptor protein levels by Western blot analysis. We conclude that potassium depletion selectively increases the expression of the B subtype of α₂-AR with no detectable effect on α(2A)-AR expression.