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This Article Full Text Full Text (PDF) All Versions of this Article: 572/1/155    most recent jphysiol.2006.105635v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by O'Connor, S. J. Articles by Giussani, D. A. Search for Related Content PubMed PubMed Citation Articles by O'Connor, S. J. Articles by Giussani, D. A. Related Collections Integrative

¹ Department of Physiology, University of Cambridge, Cambridge CB2 3EG, UK

This study investigated, in vivo, the mechanisms underlying the development of cardiovascular function in the horse fetus, with particular relevance to baroreflex function and hind limb vascular arterial reactivity to constrictor agonists. Under general anaesthesia, vascular catheters were inserted and a Transonic flow probe was implanted around one of the metatarsal arteries of 13 horse fetuses, either at 0.6 of gestation (n= 6) or at 0.9 of gestation (n= 7, term 335 days). At least 5 days after surgery, pressor, vasoconstrictor and cardiac chronotropic responses to exogenous bolus doses of phenylephrine, angiotensin II and arginine vasopressin were recorded. Fetal cardiac baroreflex slopes were obtained using the peak pressor and heart rate responses to increasing doses of phenylephrine. Fetal treatment with phenylephrine, angiotensin II and vasopressin produced significant changes in arterial blood pressure, hind limb vascular resistance and heart rate. Pressor and vasopressor responses to all agonists were greater at 0.9 than at 0.6 of gestation; however, fetal cardiac baroreflex sensitivity decreased with advancing gestational age. Correlation analysis revealed that fetal plasma cortisol rather than gestational age was a greater determinant of pressor and vasopressor reactivity. In contrast, gestational age rather than cortisol better determined heart rate and baroreflex responsiveness in the equine fetus. The data show that development of cardiovascular function in the equine fetus occurs via cortisol-dependent and -independent pathways.

(Received 18 January 2006; accepted after revision 7 February 2006; first published online 9 February 2006)
Corresponding author D. A. Giussani: Department of Physiology, University of Cambridge, Cambridge CB2 3EG, UK. Email: dag26{at}cam.ac.uk