Decreased Expression of Arginase II in the Kidneys of Dahl Salt-Sensitive Rats.

DOI PubMed 被引用文献5件 参考文献54件
  • IWATA Sachiyo
    Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medical Science
  • TSUJINO Takeshi
    Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medical Science
  • IKEDA Yoshihiro
    Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medical Science
  • ISHIDA Tatsuro
    Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medical Science
  • UEYAMA Tomomi
    Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medical Science
  • GOTOH Tomomi
    Department of Molecular Genetics, Kumamoto University School of Medicine
  • MORI Masataka
    Department of Molecular Genetics, Kumamoto University School of Medicine
  • YOKOYAMA Mitsuhiro
    Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medical Science

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Arginase catalyzes the hydrolysis of arginine to urea and ornithine. Urea is not only an important solute for concentrating urine but also inhibits Na-K-2Cl cotransport. To elucidate the roles of arginase in the development of salt-sensitive hypertension, we examined arginase activity and expression in the kidney and other organs of Dahl⁄Rapp salt-sensitive (SS) and salt-resistant (SR) rats before and after 4 weeks’ administration of a 4% NaCl or control diet. At 4 weeks of age, arginase activity in the kidney was lower in SS rats than in SR rats. Kidney arginase activity was lower in SS rats than in SR rats at 8 weeks of age, and salt loading did not alter arginase activity. Arginase II (the dominant isoform in the kidney) mRNA and protein in the kidney of salt-loaded SS rats were also lower than those of salt-loaded SR rats. Arginase activities in the liver and cerebellum did not differ between SS and SR rats. To examine the effect of urea, the product of arginase reaction, on the development of hypertension, SS rats were given a 4% NaCl diet containing 5% kaolin or 5% urea. Six-week urea supplementation attenuated the development of hypertension in SS rats. These findings suggest that decreased arginase expression in the kidney may be at least partially responsible for the salt-sensitive hypertension in SS rats. (Hypertens Res 2002; 25: 411-418)

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