Key result
A high-salt diet increased renal APN transcript and protein abundance approximately 2-fold in Sprague-Dawley and Lewis rats (P<0.05), but not in Dahl salt-sensitive rats.
Why the study?
Does a high-salt diet regulate renal Aminopeptidase N in salt-sensitive and salt-resistant rats?
Does a high-salt diet regulate renal Aminopeptidase N in salt-sensitive and salt-resistant rats?
The failure to upregulate renal Aminopeptidase N in response to a high-salt diet suggests the APN gene is a candidate for salt-sensitivity in Dahl SS/Jr rats.
Aminopeptidase N (APN) is an abundant metallohydrolase in the brush border of kidney proximal tubule cells that degrades angiotensin III (Ang III) to angiotensin IV (Ang IV) and, along with dipeptidylaminopeptidase, degrades Ang IV. We examined the impact of a high-salt diet on renal APN activity and transcript abundance in the Sprague-Dawley and Dahl salt-sensitive (SS/Jr) rat strains. APN transcript abundance and protein abundance were approximately 2-fold greater (P<0.05; n=6) in the kidneys of Sprague-Dawley and Lewis rats ingesting 8% versus 0.3% salt diets, suggesting that increased aminopeptidase activity may contribute to decreased renal sodium uptake during adaptation to a high-salt diet. In contrast, renal APN transcript abundance and activity were the same in Dahl SS/Jr rats ingesting 8.0% versus 0.3% salt diets. The APN gene was mapped, using a radiation-hybrid panel, to known quantitative loci on chromosome 1 for blood pressure in the Dahl SS/Jr rat. The results suggest that the APN gene is a good candidate for salt-sensitivity in the Dahl SS/Jr rat.
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Farjah et al. (2004) studied Hypertension. High-salt diet vs. 0.3% salt diet was evaluated on Renal APN transcript and protein abundance (2-fold greater, p=<0.05). A high-salt diet increased renal APN transcript and protein abundance approximately 2-fold in Sprague-Dawley and Lewis rats (P<0.05), but not in Dahl salt-sensitive rats.
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