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Am J Physiol Regul Integr Comp Physiol 296: R603-R609, 2009. First published December 24, 2008; doi:10.1152/ajpregu.90624.2008
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HEMODYNAMICS AND CARDIORENAL INTEGRATION

Is baroreflex control of sympathetic activity and heart rate active in the preterm fetal sheep?

Lindsea C. Booth, Simon C. Malpas, Carolyn J. Barrett, Sarah-Jane Guild, Alistair J. Gunn, and Laura Bennet

Fetal Physiology and Neuroscience Group and Circulatory Control Laboratory, Department of Physiology, University of Auckland, Auckland, New Zealand

Submitted 23 July 2008 ; accepted in final form 19 December 2008

The arterial baroreflex is a fundamental reflex that buffers rapid changes in arterial blood pressure (BP) via regulation of the heart rate and sympathetic nerve activity to the vasculature. In adults a sigmoidal relationship between BP and both heart rate and sympathetic nerve activity is well documented. Its role in blood pressure control before birth is unclear. Preterm babies have a high incidence of low BP, especially in the first few days of life, which could be related, in part, to immaturity of the baroreflex. In the present study, we investigated the baroreflex control of fetal heart rate and renal sympathetic nerve activity (RSNA) in preterm fetal sheep in utero (102 ± 1 days of gestation; term 140 days). Phenylephrine was associated with a significant increase in BP from 38 ± 2 to 58 ± 3 mmHg and a decrease in heart rate (HR) from 177 ± 4 to 116 ± 8 beats per minute (bpm). Sodium nitroprusside was associated with a significant fall in BP from 38 ± 2 to 26 ± 1 mmHg and an increase in HR from 182 ± 4 to 274 ± 8 bpm. However, the time between the 50% changes in BP and HR was significantly greater after hypotension than hypertension (31 ± 8 s vs. 14 ± 5 s, P < 0.05). No significant changes in RSNA occurred with either stimulus. This suggests that there are different maturational tempos for the components of the central autonomic response to altered blood pressure.

telemetry; renal sympathetic nerve



Address for reprint requests and other correspondence: L. Bennet, Fetal Physiology and Neuroscience Group, Dept. of Physiology, The Univ. of Auckland, Private Bag 92019, Auckland, New Zealand (e-mail: l.bennet{at}auckland.ac.nz)







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