Baroreflex and chemoreflex control of fetal hormone secretion.
In recent years, the expanding literature in fetal cardiovascular physiology and endocrinology has improved our understanding of the afferent mechanisms involved in the reflex hormonal and neural responses to cardiovascular distresses, such as hypotension, hypoxia, hypercapnia, and asphyxia. For some endocrine systems, the relative roles of peripheral and central baroreceptors and chemoreceptors are well understood. The best example of such a system is AVP, summarized in Fig. 6. Published experiments have demonstrated that AVP secretion is influenced by arterial baroreceptors, but not by arterial chemoreceptors. On the other hand, there is most likely a chemosensitive area within the central nervous system controlling AVP secretion which responds to hypoxia as well as hypercapnia. Cardiac receptors are less important in the control of AVP secretion in fetal life than in postnatal life. Our understanding of the control of other hormonal systems, including renin and ACTH, is less complete. The challenge for the future in this field will be to fill in the gaps in our knowledge of these fetal reflexes, and to provide a functional understanding of the mechanisms underlying the quantitative differences between fetus and adult. For example, does the rearrangement of the circulation at birth 'activate' the cardiac receptors by changing intracardiac pressures, or are the neuronal pathways poorly developed in the fetus compared with the postnatal animal? Also, what is the mechanism of the chemoreflex control of AVP which is independent of peripheral chemoreceptor integrity in the fetus? The answers to these questions and others will significantly improve our understanding of fetal cardiovascular and endocrine physiology. These answers will also provide information which will prove to be of practical importance in a modern age of obstetrics, paediatrics, and surgery, where the fetus will increasingly be treated as a young patient.
Wood
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Department of Physiology, University of Florida College of Medicine, Gainesville 32610-0274, USA.
D000818:Animals; D001794:Blood Pressure; D002628:Chemoreceptor Cells / Q000502:physiology*; D005333:Fetus / Q000502:physiology*; D006352:Heart Ventricles / Q000196:embryology; D006728:Hormones / Q000378:metabolism*; D006801:Humans; D011311:Pressoreceptors / Q000502:physiology*; D016276:Ventricular Function
D006728:Hormones