B0AT1, a novel member of the Na+-dependent neurotransmitter transporter family (SLC6), plays a major role in the uptake of luminal neutral amino acids. The present study evaluated the effect of high salt intake on the renal and intestinal expression of the B0AT1 transporter in SHR and WKY rats at 4 and 12 weeks of age. Rats were fed normal (NS) or high (HS - 1% saline as drinking water) salt diet for 24 h. B0AT1 transcript abundance was evaluated by quantitative real-time PCR, and data was normalized to the expression GAPDH. At 4 and 12 weeks of age, the abundance of renal B0AT1 transcript in SHR was 49% and 32% that in WKY, respectively. However, no significant differences were observed on the intestinal B0AT1 transcript abundance between SHR and WKY. HS intake decreased by ~30% B0AT1 transcript abundance in both 4- and 12-week old WKY and in 4-week old SHR. Surprisingly, HS intake produced a significant increase (45% augment) in B0AT1 mRNA in 12-week old SHR. It is concluded that under-expression of renal Na+-dependent B0AT1 amino acid transporter in SHR is organ specific and precedes the onset of hypertension. Overexpression of the Na+-dependent B0AT1 transporter at the kidney level during HS intake in adult SHR reveals their inability for adequate sodium handling when hypertension is well established. Supported by grant POCI/SAU-OBS/57916/2004.