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  Vol. 88 No. 5, NOVEMBER 1951 TABLE OF CONTENTS
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EFFECT OF VASOPRESSIN (PITRESSIN®)-INDUCED WATER RETENTION ON SODIUM EXCRETION

BERNARD C. HOLLAND, M.D.; EUGENE A. STEAD, Jr., M.D.

AMA Arch Intern Med. 1951;88(5):571-580.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

THE EXCRETION of water is influenced by many factors. One of the most important factors is the antidiuretic hormone of the posterior lobe of the pituitary gland (ADH). An increase in the osmotic activity of the blood increases the secretion of antidiuretic hormone and results in a concentrated urine.1 Drugs and reflex stimuli also release the antidiuretic hormone.2 A decreasing osmotic activity of the blood inhibits the release of the antidiuretic hormone, and a water diuresis follows.

Small intravenous doses of vasopressin injection (pitressin®) in man produce the same effect on the excretion of water and salt as does endogenously produced vasopressin. Both act by increasing the tubular absorption of water without altering glomerular filtration or renal blood flow; neither have demonstrated in short-term experiments a striking effect on excretion of sodium chloride.3 In water-loaded subjects administration of vasopressin may cause a slight decrease in the excretion . . . [Full Text PDF of this Article]


Author Affiliations

DURHAM, N. C.

From the Department of Medicine, Duke University School of Medicine.


Footnotes

This work was supported by grants from the Life Insurance Medical Research Fund and the Anna H. Hanes Memorial Fund.

Part of this work was completed during tenure of Public Health Service Fellowship of the National Institutes of Health, United States Public Health Service (Dr. Holland).



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