Expression of sulphonylurea receptor protein in mouse kidney

• Published in: Pflügers Archiv 1999-06, Vol.438 (1), p.1-7
• Main Authors: Beesley, A H, Qureshi, I Z, Giesberts, A N, Parker, A J, White, S J
• Format: Article
• Language: English
• Subjects: Amino Acid Sequence; Animals; ATP-Binding Cassette Transporters; Blotting, Western; Cricetinae; DNA Primers; Immunohistochemistry; Isomerism; Kidney - metabolism; Kidney - physiology; Kidneys; Male; Mice; Molecular Sequence Data; Potassium Channels - biosynthesis; Potassium Channels - genetics; Potassium Channels, Inwardly Rectifying; Proteins; Rats; Receptors, Drug - biosynthesis; Receptors, Drug - genetics; Reverse Transcriptase Polymerase Chain Reaction; Rodents; Sulfonylurea Receptors
• ISSN: 0031-6768; 1432-2013
• DOI: 10.1007/s004240050872

The sulphonylurea receptor (SUR) is the site of action for sulphonylurea derivatives such as glibenclamide, which are widely used as oral hypoglycaemic agents. Sulphonylureas have also been shown to affect urine flow and salt excretion by the kidney; therefore, the use of these drugs may have important implications for the pharmacological manipulation of renal salt handling. The purpose of the present investigation was to increase our understanding of the possible role of SUR in the regulation of renal function by determining the distribution of SUR isoforms within mouse kidney. Immunostaining with anti-SUR antisera revealed specific staining of SUR2B in distal nephron segments of mouse kidney. A diffuse, low level staining was observed in proximal tubules in the inner cortical region. No evidence was found for the presence of SUR2B in intra-renal blood vessels. Reverse-transcription polymerase chain reaction and Western blotting experiments indicated that SUR2B is the only known isoform expressed. These data demonstrate that SUR2B in mouse kidney is expressed in tubule regions that are critical in determining renal salt excretion.