THE PROBLEM OF CLINICAL VASOPRESSIN RESISTANCE: IN VITRO STUDIES
Authors: R M HAYS, A LEAF
Journal: Annals of Internal Medicine (1961)

Article1 April 1961THE PROBLEM OF CLINICAL VASOPRESSIN RESISTANCE: IN VITRO STUDIESRICHARD M. HAYS, M.D., ALEXANDER LEAF, M.D.RICHARD M. HAYS, M.D.Search for more papers by this author, ALEXANDER LEAF, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-54-4-700 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn recent years, there has been considerable progress in our understanding of the role of antidiuretic hormone in the renal concentrating mechanism. Studies by Hargitay and Kuhn,1 Wirz,2 Gottschalk,3 and others4-6 have led to our present picture of the mammalian nephron as an efficient countercurrent system. A concentrated urine is formed when antidiuretic hormone alters the permeability of renal tubular cells, permitting the tubular urine to come rapidly into osmotic equilibrium with the hypertonic interstitial fluid of the renal medulla.Under certain conditions, however, an apparent resistance to the action of antidiuretic hormone may develop. Despite the administration of large...Bibliography1. HargitayKuhn BW: Das multiplikations-prinzip als grundlage der harnkonzentrierung in der niere. Z. Elektrochem. 55: 539, 1951. Google Scholar2. Wirz H: The location of antidiuretic action in the mammalian kidney in the neurohypophysis, in Proceedings of the Eighth Symposium of the Colston Research Society. Edited by Heller, H. Butterworth Scientific Publications, London, p. 157, 1956. Google Scholar3. GottschalkMylle CWM: Micropuncture study of the mammalian urinary concentrating mechanism: evidence for the countercurrent hypothesis. Amer. J. Physiol. 196: 927, 1959. 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CrossrefMedlineGoogle Scholar10. LeafDempsey AE: Some effects of mammalian neurohypophyseal hormones on metabolism and active transport of sodium by the isolated toad bladder. J. Biol. Chem. 235: 2160, 1960. CrossrefMedlineGoogle Scholar11. LeafBartterSantosWrong AFCRFO: Evidence in man that urinary electrolyte loss induced by pitressin is a function of water retention. J. Clin. Invest. 32: 868, 1953. CrossrefMedlineGoogle Scholar12. DavisHallowelHyatt JODSRE: Effect of chronic pitressin administration on electrolyte excretion in normal dogs and dogs with experimental ascites. Endocrinology 55: 409, 1954. CrossrefMedlineGoogle Scholar13. LevinskyDavidsonBerliner NGDGRW: Change in urine concentration during prolonged administration of vasopressin and water. Amer. J. Physiol. 196: 451, 1959. CrossrefMedlineGoogle Scholar14. JaenikeWaterhouse JRC: The effects of sustained vasopressin stimulation in man. Clin. Res. 7: 272, 1959. Google Scholar15. SchwartzRelman WBAS: Metabolic and renal studies in chronic potassium depletion resulting from overuse of laxatives. J. Clin. Invest. 32: 258, 1953. CrossrefMedlineGoogle Scholar16. LamdinLeaf EA: Unpublished data. Google Scholar17. WirzHargitayKuhn HBW: Lokalisation des konzentrierungs prozesses in der niere durch direkte kryoskopie. Helv. Physiol. Pharmacol. Acta 9: 196, 1951. MedlineGoogle Scholar18. MafflyHaysLamdinLeaf RHRMEA: The effect of neurohypophyseal hormone in the permeability of the toad bladder to urea. J. Clin. Invest. 39: 630, 1960. CrossrefMedlineGoogle Scholar19. Leaf A: Some actions of neurohypophyseal hormones on a living membrane. J. Gen. Physiol. 43: 175, 1960. CrossrefMedlineGoogle Scholar20. HaysLeaf RA: Unpublished results. Google Scholar21. HufWills EGJ: Influence of some inorganic cations on active salt and water uptake by isolated frog skin. Amer. J. Physiol. 167: 255, 1951. CrossrefMedlineGoogle Scholar22. Ussing HH: The frog skin potential. J. Gen. Physiol. 43: 135, 1960. CrossrefMedlineGoogle Scholar23. Koefoed-JohnsenUssing VHH: Nature of the frog skin potential. Acta Physiol. Scand. 42: 298, 1958. CrossrefMedlineGoogle Scholar24. ManitiusLevitinBeckEpstein AHDFH: On the mechanism of impairment of renal concentrating ability in potassium deficiency. J. Clin. Invest. 39: 684, 1960. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication November 17, 1960.Presented in part at the Forty-first Annual Session of The American College of Physicians, San Francisco, April 4-8, 1960.From the Departments of Medicine, Harvard Medical School and the Massachusetts General Hospital, Boston, Massachusetts.†Supported by grants from the John A. Hartford Foundation, Inc., the United States Public Health Service (Grant H-2822), and the American Heart Association, Inc.‡Postdoctorate Research Fellow of the American Heart Association, Inc., 1959-1960. Present address: Department of Medicine, Albert Einstein College of Medicine, New York, New York.§Investigator, Howard Hughes Medical Institute.Requests for reprints should be addressed to Alexander Leaf, M.D., Massachusetts General Hospital, Boston 14, Massachusetts. 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KEDES, M.D., JAMES V. BONESSI, M.D., T. S. DANOWSKI, M.D., F.A.C.P.The cellular mode of action of antidiuretic hormoneEvidence for ‘Electrogenic’ Active Sodium Transport in an Epithelial MembraneWATER BALANCE AND THE PITUITARY GLAND: A REVIEWThe Clinical and Physiologic Significance of the Serum Sodium ConcentrationReversible defect in renal concentrating mechanism in patients with hypercalcemiaDer renale Diabetes insipidus in der polyurischen Phase des akuten Nierenversagens 1 April 1961Volume 54, Issue 4Page: 700-709KeywordsAntidiuretic hormoneHeartHospital medicineInterstitial fluidMedical servicesNephronsTubular cellsUrineVasopressin Issue Published: 1 April 1961 PDF DownloadLoading ...