ArticleMolecular and cellular biochemistry2007
Organ specific underexpression renal of Na+-dependent B0AT1 in the SHR correlates positively with overexpression of NHE3 and salt intake.
Article in Molecular and cellular biochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 citing papers in PubMed, 9 citations in OpenAlex.
- Absorptive transport of amino acids by the rat colon.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Dopamine and renal function and blood pressure regulation.Comprehensive Physiology · 2011Review
- The sodium pump and cardiotonic steroids-induced signal transduction protein kinases and calcium-signaling microdomain in regulation of transporter trafficking.Biochimica et biophysica acta · 2010Review
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4 authors at 3 institutions in 3 countries.
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Abstract
The present study examines the renal and intestinal expression of Na(+)-dependent amino acid transporter B(0)AT1 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 B(0)AT1 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 B(0)AT1 transcript abundance was also evaluated. For this purpose, the cloning of rat homolog of B(0)AT1 was performed. Rat B(0)AT1 shows high sequence homology to the mouse ortholog. Renal B(0)AT1 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 B(0)AT1. The decreased B(0)AT1 expression in SHR kidney was accompanied with an increase in NHE3 expression, suggesting an impaired Na(+) uptake. HS intake decreased renal B(0)AT1 mRNA in SHR and WKY at 4 weeks of age. In 12-week-old SHR, HS intake increased renal B(0)AT1 transcript abundance. Intestinal B(0)AT1 transcript was significantly increased by HS intake, though the effect was considerably more pronounced in the SHR. It is concluded, that underexpression of B(0)AT1 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 B(0)AT1 gene transcription appears to be under the influence of Na(+) delivery, being organ specific.
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