angiotensin-i and Respiratory-Distress-Syndrome--Newborn

Topics: Adult; Angiotensin I; Angiotensin II; Capillary Permeability; Female; Humans; Hypoxia; Infant, Newborn; Kallikreins; Kinins; Lung; Male; Renin-Angiotensin System; Respiratory Distress Syndrome, Newborn

Beginning with the hypothesis that interference with the metabolic function of the lung could lead to perinatal respiratory disease, we explored the role of one of these functions, angiotensin-converting enzyme activity, in the control of the fetal and newborn circulation. Converting enzyme regulates the concentration of two peptides, bradykinin and angiotensin, important in adapting the fetus to extrauterine life. Initial studies demonstrated decreasing amounts of converting enzyme activity and a parallel decrease in vascular surface with decreasing gestational age. Because we had demonstrated that there is little converting enzyme activity at the low PO2 values of the fetus we examined the fetal-placental unit and found that the placenta is the predominant site of converting enzyme activity in utero and this activity is modulated by maternal PO2. We also found that such pathophysiological accompaniments of premature birth as chilling and acidosis can stimulate the kallikrein-kinin system into overactivity. Because the kallikrein-kinin and renin-angiotensin systems are so closely interrelated with other vasoactive substances, an imbalance in production and degradation is likely to produce some of the pathophysiology seen with premature birth, including systemic hypotension, coagulopathy and oedema.

Topics: Angiotensin I; Angiotensin II; Animals; Animals, Newborn; Blood Coagulation; Blood Pressure; Bradykinin; Fetus; Fibrinolysis; Gestational Age; Humans; Infant, Newborn; Kallikreins; Kinins; Lung; Peptidyl-Dipeptidase A; Placenta; Rabbits; Renin; Respiratory Distress Syndrome, Newborn