Lori L. Woods

Abstract

In order to study the effects of hyperosmolality on fetal renal function and to gain insight into the role of AVP in the fetal urine concentrating mechanism, two types of studies were performed. In whole animal studies 9% NaCl was injected intravenously into 8 chronically catheterized pregnant ewes of 130-135 days gestation and their fetuses, followed by a continuous infusion of 9% NaCl into the ewes. Fetal and maternal plasma osmolalities rose initially by 5% and remained elevated for the next four hours. Fetal arterial and venous pressures increased transiently. Fetal urine flow increased transiently by 73%, remained elevated for at least 10 minutes, and averaged 27% below control beyond one hour. Fetal GFR, CK, and Curea were increased transiently; fetal CNa, Ccl, and Cosm were approximately doubled for up to one hour. Fetal urine osmolality, [Na+], and [c1-] increased by 47%, 47%, and 74% respectively and remained at these levels beyond about 30 minutes. Fetal Cwater had fallen by 43% after one hour, but did not become negative, and remained constant thereafter. Fetal plasma AVP rose initially by 42% and then fell towards normal.

In six fetuses AVP was infused for two hours before and four hours after hypertonic injection, causing an average rise of 48% in plasma AVP levels. During AVP infusion fetal arterial pressure was increased by 5%. Fetal urine flow averaged 37% below control; fetal urine osmolality became slightly hypertonic by one hour and then plateaued; fetal GFR increased by 22%.

During AVP infusion fetal arterial pressure was increased by 5%. Fetal urine flow averaged 37% below control; fetal urine osrnolality became slightly hypertonic by one hour and then plateaued; fetal GFR increased by 22%. Fetal Cwaterfell to zero. After hypertonic injection fetal urine osmolality did not change, but the relative contributions of Na+ and c1- to total osrnolality increased. Fetal CNa, Cc1, and Cosrnwere elevated for the duration of the experiment. Fetal AVP levels increased an additional 27%. In five animals the AVP antagonist d(CH2) 5D-tyr(Et)VAVP was infused into the fetus for two hours before and four hours after hypertonic injection. Fetal arterial pressure was reduced an average of 3% and GFR fell by 33% but no other changes were seen in response to the antagonist. After hypertonic injection fetal arterial pressure fell to 7-10% below control. Fetal urine flow showed a transient increase of 175% and a prolonged increase of 38%. Fetal urine osmolality did not change but fetal urine [Na+] and [C1-] rose by 47% and 142%. Cosm, CNa, and CC1 showed transient increases of 170-500% and prolonged increases of 50-200%.

Binding of 3H-AVP to fetal and maternal renal medullary tissue preparations was also studied. Scatchard plots of the data yielded average KD values of 0.44 and 0.80 nM, and intercepts of 15.2 and 67.2 fmol/mg protein for fetal and maternal tissue respectively. The KD's were not significantly different.

It was concluded that the transient changes in fetal renal function after hypertonic injection appear to be due to transient increases in arterial pressure, while, except for the increases in urine [Na+] and [C1-], the prolonged changes appear to be due to the effects of elevated AVP levels. The weak response of the fetal kidney to hypertonicity relative to that of the adult appears to be due at least in part to a relatively low number of AVP receptor sites in fetal medullary tissue.

LLU Discipline

Physiology

Department

Physiology

School

Graduate School

First Advisor

Robert A. Brace

Second Advisor

Cecilia Y. Cheung

Third Advisor

Ian M. Fraser

Fourth Advisor

Gordon G. Power

Degree Name

Doctor of Philosophy (PhD)

Degree Level

Ph.D.

Year Degree Awarded

1985

Date (Title Page)

12-1984

Language

English

Library of Congress/MESH Subject Headings

Argipressin -- physiology; Fetus -- growth & development; Kidney -- physiology

Type

Dissertation

Page Count

xii, 163, 3 p.

Digital Format

PDF

Digital Publisher

Loma Linda University Libraries

Usage Rights

This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights.

Collection

Loma Linda University Electronic Theses and Dissertations

Collection Website

http://scholarsrepository.llu.edu/etd/

Repository

Loma Linda University. Del E. Webb Memorial Library. University Archives

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Physiology Commons

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