Clinical as well as experimental studies have demonstrated a 70% reduction in utero-placental blood flow in pregnancies affected by severe hypertension (13, 19). In pregnant renal hypertensive rats, propranolol administration causes a further 50% reduction in utero-placental blood flow (16). The present study on renal hypertensive rats was performed in order to explore the acute effects on central haemodynamics and utero-placental blood flow of the non-selective beta-blocker pindolol, which also has an intrinsic beta-stimulatory effect. Renal hypertension was induced by partial clamping of both renal arteries in female Wistar rats 4 weeks before pregnancy. Some 2-4 days before expected parturition, cardiac output was determined with the dye-dilution technique and blood flow to the reproductive organs with the microsphere technique, both before and after acute pindolol administration. Mean arterial pressure and heart rate were recorded continuously during the experiment. After pindolol injection, mean arterial pressure fell by 22% due to a 38% reduction in total peripheral resistance. No significant changes in cardiac output, stroke volume or heart rate were found. Placental blood flow was significantly reduced, by 30%, whereas myometrial and ovarian blood flows were reduced by only 18 and 9%, respectively. Thus, the reduction in blood supply to the reproductive organs in renal hypertensive rats after acute pindolol administration was most pronounced in the placenta. This reduction in placental flow was, however, only about half as pronounced as after propranolol, which lacks intrinsic beta-stimulatory effects. This may suggest that vasodilating beta-receptors may play an important role in the maternal placental vascular bed.