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Effects of angiotensin II in fetal sheep and modification of its actions by indomethacin.
Author(s) -
Stevenson K M,
Lumbers E R
Publication year - 1995
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1995.sp020867
Subject(s) - fetus , medicine , angiotensin ii , endocrinology , excretion , blood pressure , chemistry , sodium , pregnancy , biology , genetics , organic chemistry
1. Angiotensin II (AII) was infused I.V. into seven chronically catheterized fetal sheep (gestational age, 120‐136 days). The effects of short‐term infusions of 6 and 12 micrograms kg‐1 h‐1 for 1.5 h were compared with the effects of infusing 6 micrograms kg‐1 h‐1 for 3 or 5 days (long‐term infusion). AII produced an immediate rise in fetal arterial blood pressure (P < 0.025). When infused for 3 or 5 days, 6 micrograms kg‐1 h‐1 AII caused a greater increase in arterial blood pressure (P < 0.05). 2. Infusions of 6 micrograms kg‐1 h‐1 AII for 1.5 h had no effect on fetal placental blood flow or on flow to the fetal membranes, but after AII infusion for 3 or 5 days both flows were reduced (P < 0.01 and P < 0.005, respectively). Fetal blood gas status and pH were maintained. The only change in fetal renal function observed with short‐term infusions of AII was a rise in sodium excretion when 12 micrograms kg‐1 h‐1 AII was given (P < 0.05). Infusion of 6 micrograms kg‐1 h‐1 for 3 or 5 days also caused a rise in sodium excretion (P < 0.025) because total and proximal fractional sodium reabsorptions were depressed (P < 0.01). Infusions of AII had no effects on the volume of lung liquid produced or on its composition. 3. Administration of indomethacin to the ewe (10 mg kg‐1) and to the fetus (12 mg kg‐1), during the infusion of AII, caused a rise in maternal arterial pressure (P < 0.01) but no change in fetal arterial pressure. 4. After indomethacin, umbilicoplacental blood flow rose (P < 0.05), as did fetal arterial PO2 (P < 0.05). Fetal arterial PCO2, pH and bicarbonate levels fell (P < 0.01). Glomerular filtration rate (GFR) rose (P < 0.01); there was a natriuresis (P < 0.01), chloriuresis (P < 0.01) and a kaliuresis (P < 0.05) but urine flow rate did not change. Lung liquid flow fell (P < 0.01). 5. It is concluded that in the fetus, long‐term infusions of AII at a constant dose rate cause a progressive rise in arterial pressure. In addition, effects of AII on placental blood flow and on renal function develop. Thus, short‐term infusions of AII cannot be used to predict the renal and cardiovascular effects of sustained high levels of this peptide in the fetus.(ABSTRACT TRUNCATED AT 400 WORDS)