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체액의 수분 및 나트륨 균형

Water and Sodium Balance of Body Fluid

  • 김지홍 (연세대학교 의과대학 소아과학교실)
  • Kim, Ji-Hong (Department of Pediatrics, College of Medicine, Yonsei University)
  • 투고 : 2010.10.10
  • 심사 : 2010.10.18
  • 발행 : 2010.10.31

초록

1. 나트륨은 세포외액의 유효삼투압을 형성하는 가장 중요한 용질이며, 수분 밸런스의 이상은 혈중 삼투압의 변화와 혈중 나트륨농도의 이상(hyponatremia, hypernatremia)으로 발현된다. 2. 수분의 출입의 조절에 의하여 체액의 농도변화에 대처하는 과정을 수분 밸런스(water balance) 혹은 수분 대사(water metabolism)라 하며, 세포외 액량 특히 유효혈장량의 변화에 대처하여 체내 총 나트륨량의 출입을 조절하는 과정을 나트륨 밸런스($Na^+$ balance) 혹은 나트륨 대사($Na^+$ metabolism)라 하고 그 차이점을 정리하면 Table 1과 같다. 3. 수분 밸런스의 가장 중요한 두가지 요소는 갈증반응에 의한 수분섭취와 항이뇨호르몬(AVP)에 의한 소변으로의 수분 배출이며, AVP의 분비의 강력한 자극은 삼투압의 변화와 유효혈장량의 변화이다. 4. 나트륨 밸런스는 나트륨 섭취욕구에 의해서는 큰 영향을 받지 못하며, 주로 신장에 의한 염분배출조절에 의하며 이루어지고, 사구체 여과율과 알도스테론 분비가 신장의 나트륨 배설량을 결정하는 가장 중요한 인자이다.

The maintenance of the osmolality of body fluids within a very narrow physiologic range is possible by water balance mechanisms that control the intake and excretion of water. Main factors of this process are the thirst and antidiuretic hormon arginine vasopressin (AVP), secretion regulated by osmoreceptors in the hypothalamus. Body water is the primary determinant of the osmolality of the extracellular fluid (ECF), disorders of body water homeostasis can be divided into hypo-osmolar disorders, in which there is an excess of body water relative to body solute, and hyperosmolar disorders, in which there is a deficiency of body water relative to body solute. The sodium is the predominant cation in ECF and the volume of ECF is directly proportional to the content of sodium in the body. Disorders of sodium balance, therefore, may be viewed as disorders of ECF volume. This reviews addresses the regulatory mechanisms underlying water and sodium metabolism, the two major determinants of body fluid homeostasis for a good understanding of the pathophysiology and proper management of disorders with disruption of water and sodium balance.

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참고문헌

  1. Berl T, Schrier RW. Disorders of water metabolism. In : Schrier RW, editor. Renal and Electrolyte Disorders, 4th ed. Philadelphia: Lippincott-Raven, 1997;54.
  2. Vokes T. Water homeostasis. Ann Rev Nutr 1987;7:383-406. https://doi.org/10.1146/annurev.nu.07.070187.002123
  3. Fanestil DD. Compartmentation of body water. In : Narins RG, editor. Clinical Disorders of Fluid and Electrolyte Metabolism. New York: McGraw-Hill, 1994;3-20.
  4. Verbalis JG. Disorders of body water homeostasis. Best Pract Res Clin Endocrinol Metab 2003;17:471-503. https://doi.org/10.1016/S1521-690X(03)00049-6
  5. Ruth JL, Wassner SJ. Body composition salt and water. Pediatr Rev 2006;27:181-7. https://doi.org/10.1542/pir.27-5-181
  6. Verbalis JG. Body water and osmolality. In: Jamison RL, Wilkinson R, editors. Nephrology. London: Chapman & Hall Medical, 1997;89-94.
  7. Simpson FO. Sodium intake, body sodium, and sodium excretion. Lancet 1990;2:25-9.
  8. Fitzsimons JT. Physiology and pathophysio logy of thirst and - sodium appetite. In : Seldin DW, Giebisch G, editors. The kidney, Physiology and Pathophysiology. New York: Raven Press, 1992;1615-48.
  9. Stricker EM, Verbalis JG. Water intake and body fluids. In : Zigmond MJ, et al. editors. Fundamental Neuroscience. San Diego: Academic Press, 1999;1111-26.
  10. Robertson GL. Thirst and vasopressin function in normal and disordered states of water balance. J Lab Clin Med 1983;101:351-71.
  11. Thompson CJ, Bland J, Burd J, Baylis PH. The osmotic thresholds for thirst and vasopressin release are similar in healthy man. Clin Sci (Lond) 1986;71:651-6. https://doi.org/10.1042/cs0710651
  12. Nielsen S, Kwon TH, Christensen B. Frokiaer J, Marples D. Physiology and pathophysiology of renal aquaporins. J Am Soc Nephrol 1990;10:647-63.
  13. Knepper MA. Molecular physiology of urinary concentrating mechanism: regulation of aquaporin water channels by vasopressin. Am J Physiol 1997;272:F3-F12.
  14. Phillips PA, Rolls BJ, Ledingham JG. Angiotensin II-induced thirst and vasopressin release in man. Clin Sci(Lond) 1985,68: 669-74. https://doi.org/10.1042/cs0680669
  15. Robertson GL. Posterior pituitary. In: Felig P, et al. editors. Endocrinology and Metabolism. New York: McGraw-Hill, 1995;385- 432.
  16. Rowe JW, Shelton RL, Helderman JH. Influence of the emetic reflex on vasopressin release in man. Kid International 1979;16: 729-35. https://doi.org/10.1038/ki.1979.189
  17. Robertson GL. The regulation of vasopressin function in health and disease. Recent Prog Horm Res 1976;33:333-85.
  18. Dunn FL, Brennan TJ, Nelson AE, Robertson GL. The role of blood osmolality and volume in regulating vasopressin secretion in the rat. J Clin Invest 1973;52:3212-9. https://doi.org/10.1172/JCI107521
  19. Verbalis JG. Body sodium and extracellular fluid volume. In: Jamison R, Wilkinson R, editors. Nephrology. London: Chapman & Hall Medical, 1997;95-101.
  20. Wilkins L, Richter CP. A great craving for salt by a child with cortico-adrenal insufficiency. JAMA 1940;114:866-8. https://doi.org/10.1001/jama.1940.62810100001011
  21. Orth DN, Kovacs WJ. The adrenal cortex. In: Wilson JD, et al. editors. Williams Textbook of Endocrinology. Philadelphia: W.B. Saunders, 1998;517-664.
  22. Baylis C, Lemley KV. Glomerular filtration. In: Jamison RL, Wilkinson R, editors. Nephrology. London: Chapman & Hall, 1997;25-33.
  23. Kirchner KA, Stein JH. Sodium metabolism. In: Narins RG. editor. Clinical Disorders of Fluid and Electrolyte Metabolsim. New York: McGraw-Hill, 1994;45-80.
  24. Reeves WB, Andreoli TE. Tubular sodium transport. In: Schrier RW, editor. Diseases of the Kidney and Urinary Tract. Philadelphia: Lippincott Williams and Wilkins, 2001; 135-75.