AJP - Renal Physiology, Vol 251, Issue 1 156-F163, Copyright © 1986 by American Physiological Society
Role of arginine vasopressin in fetal renal response to hypertonicity
L. L. Woods, C. Y. Cheung, G. G. Power and R. A. Brace
We studied the effects of hyperosmolality on fetal renal function and the
role of arginine vasopressin (AVP) in these responses. NaCl (9%) was
injected intravenously into chronically catheterized ewes and their
fetuses, followed by a continuous infusion of 9% NaCl into the ewes. The
fetuses were either normal, infused with AVP, or infused with an AVP
antagonist. In normal fetuses NaCl injection caused fetal and maternal
blood osmolalities to be elevated by 10-15 mosmol/kg for 4 h with no change
in fetal blood volume; fetal plasma AVP rose 42%. Fetal arterial pressures
rose transiently by 2-10 mmHg. Fetal urine flow rose transiently by 73%
after NaCl injection and then averaged 27% below control after 1 h, whereas
fetal urine osmolality increased from 188 +/- 31 to 282 +/- 33 mosmol/kg.
In a second group of fetuses AVP infusion alone caused fetal urine
osmolality to increase by 123 +/- 39 mosmol/kg and urine flow to fall 31%,
whereas in a third group the antagonist alone had no effect on urine flow
or osmolality. After hypertonic injection into fetuses infused with AVP or
the antagonist, the transient changes were similar to those in normal
fetuses. However, the sustained increase in urine osmolality and decrease
in flow after hypertonic injection were abolished in AVP-infused and
antagonist-infused fetuses. Thus it appears that the transient changes in
fetal renal function after hypertonic injection are not AVP-induced and may
be due to transient increases in arterial pressure, whereas the prolonged
changes in urine flow and osmolality appear to be mediated by increases in
fetal plasma AVP levels.
