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Developmental changes in blood pressure and the renin-angiotensin system in pony fetuses during the second half of
A J Forhead1, F Broughton Pipkin, P M Taylor
1Department of Physiology, University of Cambridge, Cambridge CB2 3EG, UK.
Abstract:
Blood pressure, heart rate and the plasma concentrations of cortisol and components of the renin-angiotensin system were measured in chronically catheterized Pony mares (n=15) and their fetuses during the second half of gestation (day 153-336 of gestation; term is normally between day 320 and day 340 of gestation). Fetal blood pressure increased towards term with the prepartum surge in plasma cortisol concentration, and there was a correlation between fetal blood pressure and both gestational age (r = 0.88, P < 0.0005) and plasma cortisol concentration (r = 0.88, P < 0.0005). Plasma concentrations of angiotensin-converting enzyme (ACE) and angiotensinogen increased towards term in the fetus; plasma ACE correlated with gestational age (r = 0.83, P < 0.0005), plasma cortisol (r = 0.76, P < 0.005) and blood pressure (r = 0.84, P < 0.0005), whereas plasma concentrations of angiotensinogen correlated with gestational age only (r = 0.80, P <0.0005). Fetal heart rate was correlated inversely with gestational age (r = -0.67, P < 0.05), plasma ACE concentration (r = -0.58, P < 0.05) and plasma angiotensinogen concentration (r = -0.69, P < 0.05). There was a positive correlation between plasma angiotensin II and renin concentrations in the fetuses (r = 0.81, P < 0.05). No gestational changes in plasma angiotensin II or renin concentrations were observed in either the mares or fetuses. Maternal blood pressure, heart rate, plasma ACE and plasma angiotensinogen concentrations also did not change over the period of study. Therefore, in Pony fetuses, maturational changes in the activity of the renin-angiotensin system occur towards term and coincide with the prepartum cortisol surge. These changes in the fetal renin-angiotensin system may be responsible, at least in part, for the observed ontogenic increase in fetal blood pressure.
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