In the spontaneous hypertensive rat, overexpression of the renal Na+-independent L-amino acid transporter
LAT2 is organ specific, precedes the onset of hypertension, correlates negatively with plasma aldosterone, and parallels
the enhanced ability to take up L-DOPA and form renal dopamine. The present study evaluated the role of aldosterone on
transcript and protein abundance of Na+-independent and Na+-dependent amino acid transporters. Na+-independent heterodimeric
amino acid transporters LAT1/4F2hc, LAT2/4F2hc and a Na+-dependent transporter ASCT2 transcript and
protein abundance was determined in the renal cortex of normotensive Wistar rats chronically treated with aldosterone
(1.5 mg), spironolactone (200 mg) or aldosterone plus spironolactone. Aldosterone significantly increased renal cortical
LAT2 mRNA levels (45 % increase), with no changes in LAT1, 4F2hc and ASCT2 transcript levels. The effect of aldosterone
upon LAT2 mRNA levels was completely prevented by spironolactone. At the protein level, aldosterone treatment
did not significantly affect LAT1 and LAT2 expression, but markedly reduced (51 % decrease) the abundance of 4F2hc
and the urinary excretion of dopamine and DOPAC. The effect of aldosterone upon 4F2hc protein abundance was not reversed
by spironolactone. Increases in renal LAT2 transcript during chronic treatment with aldosterone occur through a
spironolactone-sensitive genomic mechanism. This effect parallels with a decrease in LAT2 functionality, resulting from
decreases in 4F2hc protein abundance, which appears to be either a non-genomic effect or an indirect effect of aldosterone.
The decrease in LAT2 functionality by aldosterone correlates well with the reduction in urinary dopamine.