Regulation of renal sympathetic nerve activity at birth.
Mazursky, Jon E., Jeffrey L. Segar, Anne Monique Nuyt, Bruce A. Smith,
Jean E. Robillard.
Department of Pediatrics and the Cardiovascular Center, The
University of Iowa, Iowa City, IA
APStracts 2:0226R, 1995.
The present studies were designed to assess the contribution of onset
of respiration, separation from the placenta and a decrease in
environmental temperature on the increase in renal sympathetic nerve
activity (RSNA) which occurs at birth. In the first series of
experiments, heart rate (HR), mean arterial blood pressure (MABP) and
RSNA were recorded in chronically-instrumented near-term fetal sheep
(n=12) before and during in-utero ventilation (V); V+oxygenation
(V+O), and V+O+ umbilical cord occlusion (V+O+CO). RSNA increased by
49+/-16% during V alone (p<0.05), while no additional changes were
seen with V+O or V+O+CO. HR and MABP did not change with any
intervention. In a second series of experiments (n=10), changes in
fetal HR, MABP and RSNA in response to in-utero cooling were
recorded. Cooling of the fetal core temperature by -3.1 +/- 0.2 C
produced a rapid and sustained increase in RSNA (330+/-155%), HR
(25+/-11%) and MABP (10+/-2%), consistent with generalized
sympathoexcitation. In a third series of studies (n=3), we found that
brain stem transection between the rostral pons and posterior
hypothalamus abolishes the increase in RSNA seen at birth. These
results suggest that cooling is a major contributor to the postnatal
rise in RSNA, and that brain centers at the level of or above the
hypothalamus are involved in mediating sympathoexcitation at birth.
Received 9 February 1995; accepted in final form 27 July 1995.
APS Manuscript Number R115-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 14 August 1995.