ALPHA(2B)-ADRENERGIC RECEPTORS - IMMUNOLOCALIZATION AND REGULATION BYPOTASSIUM-DEPLETION IN RAT-KIDNEY

Citation
Lp. Huang et al., ALPHA(2B)-ADRENERGIC RECEPTORS - IMMUNOLOCALIZATION AND REGULATION BYPOTASSIUM-DEPLETION IN RAT-KIDNEY, American journal of physiology. Renal, fluid and electrolyte physiology, 39(6), 1996, pp. 1015-1026
Citations number
42
Categorie Soggetti
Physiology
ISSN journal
03636127
Volume
39
Issue
6
Year of publication
1996
Pages
1015 - 1026
Database
ISI
SICI code
0363-6127(1996)39:6<1015:AR-IAR>2.0.ZU;2-1
Abstract
Regulation of transport processes in renal epithelial cells in respons e 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 p urpose 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 a lpha(2B)-ARs, on the distribution of receptors. We employed a method t o generate a specific antibody to the third intracellular loop of the alpha(2B)-AR and demonstrated the specificity of this antibody. Our re sults demonstrated, for the first time, evidence for the alpha(2B)-rec eptor protein in the basolateral membrane of proximal convoluted and s traight tubules. No specific immunoreactivity was detected in other ne phron segments. Finally, the increase in alpha(2B)-AR expression obser ved previously was due to the recruitment of alpha(2B)-ARs to the baso lateral membrane of proximal tubules.