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. 2011;2011:391762.
doi: 10.4061/2011/391762. Epub 2011 Apr 12.

Insulin Resistance, Obesity, Hypertension, and Renal Sodium Transport

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Free PMC article

Insulin Resistance, Obesity, Hypertension, and Renal Sodium Transport

Shoko Horita et al. Int J Hypertens. .
Free PMC article

Abstract

Sodium transport through various nephron segments is quite important in regulating sodium reabsorption and blood pressure. Among several regulators of this process, insulin acts on almost all the nephron segments and is a strong enhancer of sodium reabsorption. Sodium-proton exchanger type 3 (NHE3) is a main regulator of sodium reabsorption in the luminal side of proximal tubule. In the basolateral side of the proximal tubule, sodium-bicarbonate cotransporter (NBCe1) mediates sodium and bicarbonate exit from tubular cells. In the distal nephron and the connecting tubule, epithelial sodium channel (ENaC) is of great importance to sodium reabsorption. NHE3, NBCe1, and ENaC are all regulated by insulin. Recently with-no-lysine (WNK) kinases, responsible for familial hypertension, stimulating sodium reabsorption in the distal nephron, have been found to be also regulated by insulin. We will discuss the regulation of renal sodium transport by insulin and its roles in the pathogenesis of hypertension in insulin resistance.

Figures

Figure 1
Figure 1
The main sodium transporters and regulators in the proximal tubule and distal and connecting/collecting tubules. In the proximal tubule, insulin and Ang II stimulate NHE3 at the luminal side, NBCe1, and Na-K-ATPase at the basolateral side. In the distal and connecting/collecting tubules, insulin stimulates ENaC and NCC in the luminal side, Na-K-ATPase at the basolateral side. Insulin may also indirectly stimulate NCC via WNK kinases.
Figure 2
Figure 2
Mechanism of hypertension in insulin resistance. In insulin resistance, insulin-induced vasodilation is impaired. However, insulin induced sodium reabsorption through various nephron segments seems to be preserved or enhanced.

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