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GASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

Increased Expression of the Sodium Transporter BSC-1 in Spontaneously Hypertensive Rats

Center for Clinical Pharmacology, Departments of Pharmacology and Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania

The purpose of this study was to compare the expression of BSC-1 (bumetanide-sensitive Na⁺-K⁺-2Cl^– cotransporter) in kidneys of spontaneously hypertensive rats (SHR) versus Wistar-Kyoto (WKY) rats by immunoblotting and reverse transcription-polymerase chain reaction. To determine the specificity of any observed changes in BSC-1 expression, we also compared expression of the thiazide sensitive Na⁺-Cl^– cotransporter (TSC), the type-3 Na⁺-H⁺ exchanger (NHE-3), Na⁺-K⁺-ATPase-₁, the inwardly rectifying K⁺ channel (ROMK-1), the type-1 cotransporter (NBC-1), aquaporin-1, and aquaporin-2. Analyses were performed on outer cortex, outer medulla, and inner medulla. BSC-1 protein was detected in outer medulla and was markedly (6-fold) higher in SHR. TSC protein was detected in the cortex and was not overexpressed in SHR. Aquaporin-1 protein was detected in all three regions and was not overexpressed in SHR. Aquaporin-2 and ROMK-1 proteins were detected in all three regions, but were moderately elevated (2-fold) only in the SHR inner medulla. Na⁺-K⁺-ATPase and NHE-3 proteins were detected in all three regions. Na⁺-K⁺-ATPase-₁ was modestly (25%) increased in SHR outer and inner medulla, whereas NHE-3 was moderately (2-fold) increased in the SHR cortex and inner medulla. NBC-1 protein was detected only in the cortex and was higher (2-fold) in SHR. mRNA levels of BSC-1, aquaporin-2, and ROMK-1 were not elevated in SHR, indicating a post-translational mechanism of protein overexpression. High-dose furosemide increased fractional sodium excretion more in SHR than WKY (3-fold). We conclude that increased expression of BSC-1, and to a lesser extent, aquaporin-2, ROMK-1, NHE-3, and NBC-1 may contribute to the pathogenesis of hypertension in the SHR.

Address correspondence to: Edwin K. Jackson, Center for Clinical Pharmacology, University of Pittsburgh Medical Center, 623 Scaife Hall, 3550 Terrace Street, Pittsburgh, Pennsylvania 15261. E-mail: edj{at}pitt.edu

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