AJP - Regulatory, Integrative and Comparative Physiology, Vol 270, Issue 1 86-R93, Copyright © 1996 by American Physiological Society

ARTICLES

Regulation of renal sympathetic nerve activity at birth

J. E. Mazursky, J. L. Segar, A. M. Nuyt, B. A. Smith and J. E. Robillard
Department of Pediatrics, University of Iowa, Iowa City 52242, USA.

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) that 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), whereas 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 degree 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 increases 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.

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