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Review
. 2011:172:63-75.
doi: 10.1159/000328684. Epub 2011 Aug 30.

Regulation of sodium transport in the proximal tubule by endothelin

Ye Zhang, Pedro A Jose, Chunyu Zeng
Review

Regulation of sodium transport in the proximal tubule by endothelin

Ye Zhang et al. Contrib Nephrol. 2011.

Abstract

Human essential hypertension and rodent genetic hypertension are associated with increased sodium transport in the renal proximal tubule and medullary thick ascending limb of Henle. The proximal tubule, which secretes endothelin (ET), expresses the ET(B) receptor. Low (nM) concentrations of ET, via the ET(B) receptor, inhibit sodium and water transport and ATP-driven drug secretion in the proximal tubule. In contrast, very low (pM) and high nM concentrations of ET increase renal proximal sodium transport, but the receptor involved remains to be determined. The natriuretic effect of ET(B) receptor stimulation is impaired in spontaneously hypertensive rats, due in part to a defective interaction with D(3) dopamine and angiotensin II type 1 receptors. Impaired ET(B) receptor function in the renal proximal tubule may be important in the pathogenesis of genetic hypertension.

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Figures

Figure 1
Figure 1. Interactions among ETB (ETBR), D3 dopamine (D3R), and AT1 (AT1R) receptors in the regulation of sodium transport in the renal proximal tubule
Stimulation of the AT1R increases the activity of sodium transporters, sodium exchangers, and the sodium pump (e.g., NaHCO3 cotransporter, Na+H+exchanger, and Na+-K+-ATPase), while their activity is decreased by the stimulation of ETBR and dopamine receptors (e.g., D1R and D3R). The ETBR, D3R, and AT1R physically interact with each other. Stimulation of the ETBR increases D3R expression and function but the opposite effect occurs with AT1R expression and function. The D3R also negatively regulates AT1R expression. In contrast, stimulation of the AT1R increases ETBR expression, in the long-term, and ETBR cell surface expression, in the short-term. Thus, the ETBR synergistically interacts with the D3R to counterbalance the stimulatory effect of the AT1R on sodium transport in the renal proximal tubule.
See this image and copyright information in PMC

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