Abstract
Experiments were carried out in pregnant nephrectomized rabbits to determine the relationship between uterine blood flow and uterine renin secretion. Uterine blood flow was measured by the percentage distribution of radioactive microspheres injected into the left ventricle which lodged in uterus and placenta, and cardiac output was measured by dye dilution. In 40 animals, 24 hr after nephrectomy, uterine blood flow was 4.7+/-0.4% of cardiac output and absolute flow 32.4+/-3 ml/100 g per min. Plasma renin activity (PRA) in uterine vein, 994+/-182 ng/100 ml per hr, was higher than in carotid artery, 832+/-143 (P < 0.025). With reduction of uterine blood flow from 4.7+/-0.5 to 1.95+/-0.3% of cardiac output and absolute flow from 30.8+/-4.6 to 8.8+/-2 ml/100 g per min, uterine vein PRA rose from 1434+/-234 to 4430+/-300 (P < 0.001), and carotid artery PRA from 1009+/-200 to 2300+/-350 (P < 0.01). Hemorrhagic hypotension caused uterine vein PRA to increase from 913+/-293 to 3638+/-1276 (P < 0.001) and carotid artery PRA from 774+/-252 to 1730+/-433 (P < 0.01). Uterine blood flow expressed as a percentage of cardiac output remained constant after hemorrhage, 5.5+/-0.9 and 6.3+/-0.8%, although absolute flow fell from 37+/-7.7 to 29+/-3.6 ml/100 g per min because of the large fall in cardiac output which occurred.Angiotensin, 10 ng/kg per min, caused no significant change in blood pressure or cardiac output but increased uterine blood flow from 4.1+/-0.6 to 8.4+/-1% (P < 0.005) of cardiac output with absolute flow increasing from 37.4+/-7 to 73.2+/-10 ml/100 g per min (P < 0.001). The increase in uterine blood flow during angiotensin was abolished by the prior administration of propranolol. Isoproterenol, 0.5 mu/min, increased uterine blood flow from 3.5+/-0.6 to 6.4+/-1.2% of cardiac output (P < 0.02) with absolute flow increasing from 25+/-5 to 51+/-12 ml/100 g per min (P < 0.05). Norepinephrine, 500 ng/min, caused no significant change in uterine blood flow. These findings suggest that uterine renin might be involved in regulating uterine blood flow, secretion being increased in response to a reduction in flow with the resultant rise in circulating or local angiotensin, through beta adrenergic stimulation, increasing uterine blood flow.