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  Vol. 106 No. 2, August 1963 TABLE OF CONTENTS
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Control of Water Balance in the Newborn

D. A. FISHER, MD; H. R. PYLE, JR, AB; J. C. PORTER; A. G. BEARD, MD; T. C. PANOS, MD

Am J Dis Child. 1963;106(2):137-146.

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 homeostatic capabilities and limitations of the newborn infant have been intensely studied in recent years. With increasing knowledge, the over-all effectiveness of neonatal reactivity in this respect becomes more impressive. However, responses related to renal function and especially to antidiuretic hormone (ADH) secretion and control of water excretion remain to be worked out in detail. Renal function during the neonatal period is characterized by a low maximal tubular excretory capacity with a relatively high filtration fraction, low rate of solute excretion, low urine flow rates, limited capacity to concentrate urine, and delayed excretion of water loads. Several scholarly reviews have summarized the accumulated data on this subject.1-7

Investigations of the response to thirsting, water loading, and vasopressin (Pitressin) administration have shown the newborn infant to be able to respond with increases and decreases of urine osmolality, indicating the capacity for ADH secretion and renal tubular response to ADH, . . . [Full Text PDF of this Article]


Author Affiliations

LITTLE ROCK, ARK

D. A. Fisher, MD, Assistant Professor, Department of Pediatrics, University of Arkansas Medical Center, Little Rock, Ark.; Assistant Professor of Pediatrics (Dr. Fisher); fourth-year medical student, research fellowship (Mr. Pyle); third-year medical student, research fellowship (Mr. Porter); Associate Professor of Pediatrics (Dr. Beard); Professor and Chairman of Pediatrics (Dr. Panos).; Department of Pediatrics, University of Arkansas School of Medicine.


Footnotes

Presented in part before the Southern Society for Pediatric Research, Gainesville, Fla, Nov 9-10, 1962.

Supported by Grants A-4822 and A-3174 from the National Institutes of Arthritis and Metabolic Disease and NIH General Research Support Grant 1-GS-51.



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