Hypertension-linked mutation in the adducin alpha-subunit leads to higher AP2-mu2 phosphorylation and impaired Na+,K+-ATPase trafficking in response to GPCR signals and intracellular sodium.

@article{Efendiev2004HypertensionlinkedMI,
  title={Hypertension-linked mutation in the adducin alpha-subunit leads to higher AP2-mu2 phosphorylation and impaired Na+,K+-ATPase trafficking in response to GPCR signals and intracellular sodium.},
  author={Riad Efendiev and Rafael T Krmar and Goichi Ogimoto and Jean Zwiller and G. D. Tripodi and Adrian I. Katz and Giuseppe Bianchi and Carlos Humberto Pedemonte and Alejandro Mario Bertorello},
  journal={Circulation research},
  year={2004},
  volume={95 11},
  pages={1100-8}
}
Alpha-adducin polymorphism in humans is associated with abnormal renal sodium handling and high blood pressure. The mechanisms by which mutations in adducin affect the renal set point for sodium excretion are not known. Decreases in Na+,K+-ATPase activity attributable to endocytosis of active units in renal tubule cells by dopamine regulates sodium excretion during high-salt diet. Milan rats carrying the hypertensive adducin phenotype have a higher renal tubule Na+,K+-ATPase activity, and their… CONTINUE READING

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