Several clinical and animal studies suggest that "blood pressure goes with the kidney," that is, a normotensive recipient of a kidney genetically programmed for
hypertension will develop
hypertension. Intrarenal
dopamine plays an important role in the pathogenesis of
hypertension by regulating epithelial
sodium transport. The candidate transport systems for
L-DOPA, the source for
dopamine, include the
sodium-dependent systems B(0), B(0,+), and y(+)L, and the
sodium-independent systems L (LAT1 and LAT2) and b(0,+). Renal LAT2 is overexpressed in the prehypertensive spontaneously hypertensive rat (SHR), which might contribute to enhanced
L-DOPA uptake in the proximal tubule and increased
dopamine production, as an attempt to overcome the defect in D1 receptor function. On the other hand, it has been recently reported that impaired
arginine transport contributes to low renal
nitric oxide bioavailability observed in the SHR renal medulla. Here we review the importance of renal
amino acid transporters in the kidney and highlight pathophysiological changes in the expression and regulation of these transporters in
essential hypertension. The study of the regulation of renal
amino acid transporters may help to define the underlying mechanisms predisposing individuals to an increased risk for development of
hypertension.