Renal, hormonal, and cardiovascular responses to chronic angiotensin I infusion in the ovine fetus

Abstract

Long-term infusion of angiotensin I (ANG I) into the ovine fetus has been shown to cause excess accumulation of fetal fluid in the allantoic compartment. It was hypothesized that this resulted from sustained increases in fetal urine production, and the hormonal basis was examined. ANG I (6.7 micrograms/h, n = 6) or isotonic saline (n = 6) was infused for 3 days into chronically cannulated ovine fetuses (112-122 days of gestation). ANG I caused an immediate and progressive increase in mean arterial blood pressure (from 42 +/- 2 to 57 +/- 4 mmHg), increased urine flow rate (from 15 +/- 3 to 48 +/- 8 ml/h), and increased glomerular filtration rate (from 97 +/- 15 to 146 +/- 24 ml/h), without significant changes in fetal plasma concentrations of aldosterone, atrial natriuretic factor (ANF), adrenocorticotropin, or cortisol. There were substantial increases in sodium and chloride excretion, due to both increased fetal urine concentrations and fetal urine flow, without significant changes in urine osmolality (from 134 +/- 9 to 147 +/- 12 mosmol/kg water). There were no significant changes in any parameter in the saline-infused fetuses. Neither amniotic or allantoic fluid volume was significantly changed by ANG I infusion, but allantoic fluid Cl- concentration increased significantly. The conclusions are that ANG I caused a diuresis and natriuresis in the fetal sheep independent of changes in cortisol or ANF.