alpha(2B)-Adrenergic receptors: Immunolocalization and regulation by potassium depletion in rat kidney

Regulation of transport processes in renal epithelial cells in response to alpha(2)-adrenergic receptor (alpha(2)-AR) stimulation is likely due to specific effects of the A-, B-, or C-subtype alpha(2)-AR. The purpose of the present study was 1) to examine the precise localization, using subtype-specific antibodies, the B-subtype alpha(2)-AR protein, the most abundant alpha(2)-AR in rat kidney; and 2) to determine the effect of dietary potassium restriction, a factor known to increase alpha(2B)-ARs, on the distribution of receptors. We employed a method to generate a specific antibody to the third intracellular loop of the alpha(2B)-AR and demonstrated the specificity of this antibody. Our results demonstrated, for the first time, evidence for the alpha(2B)-receptor protein in the basolateral membrane of proximal convoluted and straight tubules. No specific immunoreactivity was detected in other nephron segments. Finally, the increase in alpha(2B)-AR expression observed previously was due to the recruitment of alpha(2B)-ARs to the basolateral membrane of proximal tubules.