1. Plasma arginine vasopressin (AVP), renin activity (PRA) and aldosterone (ALD) were measured immediately before and 60 min after intravenous administration of frusemide and passage from lying to standing in 10 untreated healthy subjects (group 1), eight asthmatic patients treated with prednisone (group 2) and 13 heart-transplant recipients treated with prednisone and cyclosporine (group 3). Three different tests for cardiac vagal innervation were performed in the study population. They confirmed that the patients of group 3 were denervated whereas those of groups 1 and 2 had an intact cardiac innervation.
2. Plasma volume depletion after frusemide administration estimated from the rise in plasma proteins was 10–12%. Mean blood pressure was higher in the transplant recipients but did not change in the three groups. Heart rate was also greater in the transplant recipients as a result of vagal denervation. PRA and ALD increased in all the subjects: 2.8, 3.3 and 2.2 times basal value for PRA, 2.7, 4.6 and 2.1 times basal value for ALD in groups 1, 2 and 3 respectively. In contrast, plasma AVP increased only in the two control groups (× 1.45 and × 1.65 in groups 1 and 2 respectively) whereas it was unchanged in the group of heart-transplant recipients (× 1.05).
3. In order to better understand the etiology of the high basal AVP plasma levels observed in group 3, AVP response to a standard water load was studied in eight supplementary heart-transplant recipients: 81.5% of the water load was excreted over 3 h and plasma AVP fell significantly (× 0.76).
4. These results suggest that, in humans, cardiac receptors and innervation play a dominant role in AVP response to volume depletion. In contrast, we found no evidence for a dominant role of cardiac receptors and innervation in mediating renin and aldosterone secretion.