The Role of Aldosterone in the Pathogenesis of Congestive Heart Failure

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  • ITO Teizo
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo
  • NAKAMURA Kazumichi
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo
  • KINOUCHI Takashi
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo
  • KUROSAWA Takeshi
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo
  • OHSHIMA Motochika
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo
  • NAGASAKA Masahito
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo
  • TAKAHASHI Masao
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo
  • MAEDA Teiryo
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo
  • HANAOKA Waichiro
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo
  • SEKI Kiyoshi
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo
  • YOSHITOSHI Yawara
    First Department of Internal Medicine, Faculty of Medicine, University of Tokyo

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The effect of aldosterone on electrolytes and water diuresis was examined on 3 groups of human and dog, i.e. normal, mild heart disease and congestive failure.<br>In control group, the administration of d-aldosterone prior to mannitol or saline infusion led to a large amount of potassium diuresis but did not decrease sodium excretion in urine. This phenomenon is regarded as the initial effect of aldosterone for electrolytes and water diuresis.<br>In patients and dogs with heart disease without edema, however, aldosterone showed differential effects between mannitol and saline infusion. By mannitol, potassium excretion was unchanged despite reduced sodium excretion, but by saline the former was increased and the latter was unchanged.<br>In patients and dogs with congestive heart failure, whether on mannitol or on saline, the pre-treatment of aldosterone minimized the sodium excretion in urine, but the potassium excretion was almost as same as that in normal cases and in mild heart disease.<br>These observations lead to the following conclusions.<br>(1) The increased aldosterone secretion itself is not the only necessary cause of edema.<br>(2) The sodium in renal tubules is reabsorbed by 2 ways; one is through Na-K exchange and the other is effected by the sodium reabsorption independent of Na-K exchange, and aldosterone can act on both processes differently according to the condition of patient or animal.<br>(3) The second way will act in initial effect and escape phenomenon in normal human and dog, but it will show the strong sodium retaining effect in human and dog with congestive heart failure.<br>(4) Aldosterone may probably aggravate the edema in congestive heart failure, but it might not be the primary cause of edema and its primary cause is rather the altered tubular responsiveness to aldosterone.

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