Angiotensin-converting enzyme (ACE) plays an important role in the renin-angiotensin system through catalysing angiotensin II production. In adult animals, the primary source of ACE is the pulmonary vasculature, but until birth the lungs are poorly perfused. In fetal sheep, pulmonary, renal and plasma ACE concentrations increase close to term in association with the prepartum cortisol surge (Forhead et al. 2000b). Plasma ACE concentrations have been shown to increase with gestational age and plasma cortisol in fetal foals (Forhead et al. 2000a), although the ontogeny of pulmonary and renal ACE is unknown in this species. Therefore, this study examined the ontogeny of ACE concentration in the lungs and kidneys of fetal and neonatal foals. Experiments were carried out in accordance with UK legislation. Tissues were collected from 44 foals (humanely killed with an overdose of sodium pentobarbitone (200 mg kg^-1)); ages ranged from day 100 of gestation to 7 days of postnatal age (term ¦335 days). Pulmonary and renal ACE concentrations were measured by a spectrophotometric assay (Forhead et al. 2000b) and protein content was determined by the Lowry method. Linear regression was used to compare both ACE and protein concentrations with gestational age. Fetal pulmonary ACE levels were negligible until day 250 of gestation, and rose rapidly after 300 days of gestation (Fig. 1).

The highest level of pulmonary ACE was measured in a 1-day-old foal (peak concentration = 5.88 nmol min^-1 (mg protein)^-1). Pulmonary ACE showed a positive correlation with gestational age (r = 0.77, P < 0.0001, n = 30 (log scale)). In contrast, ACE was detected in fetal kidneys from 100 days of gestation but remained unchanged towards term. There was no correlation between renal ACE and gestational age. Overall mean concentrations (± S.E.M.) of renal ACE (0.15 ± 0.03 nmol min^-1 (mg protein)^-1) were also approximately 10 times less than mean pulmonary values. There was a positive correlation between gestational age and renal protein content (r = 0.65, P < 0.0001, n = 32), but not with pulmonary protein content. These data show that pulmonary ACE increases towards term in the fetal foal. This increase may be associated with the prepartum cortisol surge that occurs very close to delivery in this species. These findings may have consequences for understanding the maturation of the renin-angiotensin system over the perinatal period in the horse and other species.