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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Issue number||2 35-2|
|State||Published - 1994|
- sodium-hydrogen exchange
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