Factors influencing plasma renin and angiotensin II in the conscious pregnant ewe and its foetus

Abstract

1. Plasma renin (measured in the presence of additional substrate) was significantly higher (10.7 +/- 1.1 S.E. of mean ng/ml.hr) in foetal lambs of 111-144 days gestation age (full term 147 days) than in their mothers (1.5 +/- 0.2 ng/ml.hr S.E. of mean, P < 0.001) but plasma angiotensin II concentrations were in the same range (ewe 47.3 +/- 6.6 S.E. of mean, foetus 47.4 +/- 14.1 S.E. of mean pg/ml.). The endogenous velocity of renin production by foetal plasma was also greater than that of maternal plasma.2. Foetal plasma [Na(+)] (137 +/- 0.8 S.E. of mean m-equiv/l.), was lower than that in the ewe (142 +/- 1.5 m-equiv/l. S.E. of mean, P < 0.01).3. Foetal plasma renin in lambs of less than 120 days gestation was lower (9.2 +/- 2.7 S.E. of mean ng/ml.hr) than that in lambs of over 130 days gestation (12.6 +/- 2.6 ng/ml.hr S.E. of mean, P < 0.01). Foetal plasma [K(+)] (3.8 +/- 0.1 S.E. of mean m-equiv/l.) was also lower in lambs of less than 120 days gestation than in those over 130 days (4.1 +/- 0.1 S.E. of mean m-equiv/l., P < 0.001).4. When small volumes of blood (</= 3% of blood volume) were withdrawn from foetal lambs, plasma renin increased. The% increase of plasma renin in hypoxaemic foetal lambs was significantly less (P < 0.05) than in control lambs. At the end of 60 min hypoxaemia, arterial pressure and plasma [K(+)] were significantly higher in hypoxaemic than in control foetal lambs.5. During foetal hypoxaemia, plasma angiotensin II concentration increased concurrently with plasma renin.6. Bilateral nephrectomy was performed in two foetal lambs. Plasma renin fell to very low levels and angiotensin II became undetectable.7. Adrenaline ( approximately .0.42 mug/min.kg I.V.) infused into the foetus did not alter foetal plasma renin. When adrenaline was infused into the ewe ( approximately 0.26 mug/min.kg) maternal plasma renin increased. Maternal infusion of adrenaline raised foetal plasma renin significantly more (P < 0.05) than foetal infusion.8. It is concluded that the foetal kidney is the major source of foetal renin in the last quarter of gestation and that renin release is stimulated by very small reductions of blood volume. Hypoxaemia does not augment renin release and cannot be responsible for high levels of renin and angiotensin associated with vaginal delivery.