Developmental changes in pulmonary and renal angiotensin-converting enzyme concentration in fetal and neonatal horses
| Autor: | A. L. Fowden, N. Holdstock, S. J. O’Connor, Alison J. Forhead, Dino A. Giussani |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Aging
medicine.medical_specialty Gestational Age Reproductive technology Peptidyl-Dipeptidase A Kidney Endocrinology Internal medicine Genetics medicine Animals Horses Lung Molecular Biology Fetus Pregnancy biology Horse Angiotensin-converting enzyme medicine.disease Blood pressure Animals Newborn Reproductive Medicine biology.protein Gestation Animal Science and Zoology Homeostasis Developmental Biology Biotechnology |
| Zdroj: | Reproduction, Fertility and Development. 14:413 |
| ISSN: | 1031-3613 |
| DOI: | 10.1071/rd02044 |
| Popis: | Angiotensin-converting enzyme (ACE) has an active role in the control of blood pressure and body fluid homeostasis both before and after birth. This study investigated the ontogeny of pulmonary and renal ACE concentrations in fetal and neonatal horses. Fetal pulmonary ACE concentration increased from 250 days towards term (c. 335 days). Newborn foals showed significantly higher mean concentrations of pulmonary ACE (4.40 +/- 0.62 nmol min(-1) mg protein(-1)) than both fetuses during late gestation (1.23 +/- 0.51 nmol min(-1) mg protein(-1)) and animals aged 1 day to 2 weeks of postnatal age (0.85 +/- 0.15 nmol min(-1) mg protein(-1)). Renal ACE was detected in fetal horses from 100 days of gestation but showed no developmental trend during the second half of gestation or in early postnatal life. Overall in the fetus, mean concentrations of renal ACE were also approximately 10 times lower than mean pulmonary values. Renal ACE concentration may be related to the functional immaturity of the equine kidneys. The increase in pulmonary ACE concentration seen towards term in the fetal horse may be induced by the prepartum cortisol surge that occurs very close to delivery in this species. Therefore, premature delivery in this species may interrupt the onset of ACE production in the fetal lungs and circumvent the normal maturation of the renin-angiotensin system. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|