| pubmed-article:2137991 | pubmed:abstractText | The fetal urine flow response to acute increases in osmolality may be mediated by changes in the plasma concentrations of atrial natriuretic factor (ANF), arginine vasopressin (AVP), and/or angiotensin II (ANG II). To explore this, hypertonic NaCl or mannitol was infused intravascularly over 10 min into chronically catheterized fetal sheep and their mothers simultaneously, followed by a 2-h maternal infusion at 1-2 ml/min to maintain the elevated osmolality. Fetal osmolality rose by 16 mosmol/kgH2O during 13% mannitol and 2.5% NaCl infusions and by 57 mosmol/kgH2O during 7% NaCl infusions. Large increases in fetal urine flow occurred in the three groups with peak flows (average of 304%, P less than 10(-6)) at 0-4 min after the end of the infusion. Flow declined to preinfusion values in all groups at 30-40 min. These changes in urine flow occurred in parallel with a rise (to 223%, P less than 10(-6)) and fall in plasma ANF concentrations. One hour after the infusions, urine flow declined to 50% of control concomitant with elevations in plasma AVP (to 414%, P less than 10(-6)), whereas plasma ANG II concentration did not change. Thus the initial increase in fetal urine flow in response to acute hypertonic infusions is temporally related to a rise in fetal plasma ANF, whereas the subsequent fall in urine flow is temporally related to a fall in plasma ANF and a simultaneous rise in AVP concentration. This suggests that ANF may contribute to the acute urine flow increase after hypertonic infusion, whereas AVP appears to be more important for the long-term regulation of fetal urine flow. | lld:pubmed |
