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Organ specific underexpression renal of Na+-dependent B0AT1 in the SHR correlates positively with overexpression of NHE3 and salt intake

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Abstract

The present study examines the renal and intestinal expression of Na+-dependent amino acid transporter B0AT1 during the development of hypertension in the spontaneous hypertensive rats (SHR) and its normotensive control (Wistar-Kyoto rat; WKY), and evaluates whether the expression of renal B0AT1 correlates with changes in the expression of Na+ transporters, type 3 Na+/H+ exchanger (NHE3) and Na+–K+-ATPase, known to occur in the SHR. The effect of high salt (HS) intake on the expression of renal and intestinal B0AT1 transcript abundance was also evaluated. For this purpose, the cloning of rat homolog of B0AT1 was performed. Rat B0AT1 shows high sequence homology to the mouse ortholog. Renal B0AT1 transcript abundance was lower in SHR than WKY at both 4 and 12 weeks of age. No significant differences between strains were observed in terms of intestinal expression of B0AT1. The decreased B0AT1 expression in SHR kidney was accompanied with an increase in NHE3 expression, suggesting an impaired Na+ uptake. HS intake decreased renal B0AT1 mRNA in SHR and WKY at 4 weeks of age. In 12-week-old SHR, HS intake increased renal B0AT1 transcript abundance. Intestinal B0AT1 transcript was significantly increased by HS intake, though the effect was considerably more pronounced in the SHR. It is concluded, that underexpression of B0AT1 in the SHR kidney is organ specific, precedes the onset of hypertension and correlates negatively with the renal tubular transport of Na+. The regulation of B0AT1 gene transcription appears to be under the influence of Na+ delivery, being organ specific.

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Acknowledgements

Supported by Fundação para a Ciência e a Tecnologia, POCI, FEDER and Programa Comunitário de Apoio (POCI/SAU-OBS/57916/2004).

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Correspondence to Patrício Soares-da-Silva.

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Pinho, M.J., Serrão, M.P., José, P.A. et al. Organ specific underexpression renal of Na+-dependent B0AT1 in the SHR correlates positively with overexpression of NHE3 and salt intake. Mol Cell Biochem 306, 9–18 (2007). https://doi.org/10.1007/s11010-007-9548-9

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