1. Thirty-three insulin-dependent diabetic patients were separated into two groups from the results of three different tests for cardiac vagal neuropathy: heart rate response to deep breathing, Valsalva manoeuvre and heart rate response to postural change. Seventeen patients were considered as without ('intact’ patients) and 16 as with ('denervated’ patients) cardiac autonomic dysfunction. One patient with a transplanted heart was also studied.
2. Plasma antidiuretic hormone (ADH), plasma aldosterone and plasma renin activity (PRA) were measured immediately before and 60 min after intravenous administration of frusemide and passage from lying to standing. The kinetics of hormonal responses were analysed more precisely (five blood collections) in six patients of each group who were studied again. Heart rate and blood pressure were recorded before each blood collection.
3. Volume depletion estimated from the rise in plasma protein (+ 11.9 and + 12.2% in ‘denervated’ and ‘intact’ patients respectively) and heart rate response (+ 10.6 and + 14.7%) were similar in both groups. Mean blood pressure was unchanged in the ‘intact’ patients whereas it fell in the ‘denervated’ patients (−13.5%). PRA (+ 161.5 and + 231.2% in ‘denervated’ and ‘intact’ patients respectively) and plasma aldosterone (+ 318.2 and 279%) increased in both groups whereas plasma ADH was stimulated only in ‘intact’ patients (+ 55.3%). The failure of ADH to respond significantly to the volume stimulus in ‘denervated’ patients was confirmed by the results of the time-course study. Plasma ADH remained at the same levels in ‘denervated’ patients whereas it increased significantly (+ 82.4%) in ‘intact’ patients. There was no ADH response in the transplanted patient.
4. These results suggest that, in humans, cardiac receptors and vagal pathways play a role in ADH response to volume depletion.