EVIDENCE THAT THE ACUTE CARDIOVASCULAR-RESPONSE TO ISOPRENALINE IS PARTLY MEDIATED VIA RENIN RELEASE

1. The possible effect of the increased plasma renin activity induced by β-adrenoreceptor stimulation in supporting arterial pressure has been studied in five normal subjects on a diet of 100 mmol of sodium/day for 4 days or 40 mmol of sodium/day for 4 days by infusing isoprenaline at 1.0, 2.0 or 3.0 μg min-1 70 kg-1, each for 1 h with 45 min between each infusion rate. During the last 30 min of each isoprenaline dose, the angiotensin II analogue [Sar1,Ala8]angiotensin II (saralasin) was infused. 2. Isoprenaline significantly (at least P < 0.05) increased the pulse rate, systolic arterial pressure and plasma renin activity; the diastolic blood pressure decreased but the mean arterial pressure did not change. Saralasin administered to subjects on the 100 mmol of sodium/day diet significantly (at least P < 0.05) lowered mean arterial pressure at the two highest isoprenaline infusion rates. 3. With patients on a low sodium diet, saralasin lowered mean arterial pressure at all three isoprenaline infusion rates. On the low sodium diet the fall in mean arterial pressure caused by saralasin was significantly greater (P < 0.05) at the isoprenaline infusion rate of 3.0 μg min-1 70 kg-1 than at the infusion rate of 1.0 μg min-1 70 kg-1. The change in mean arterial pressure with saralasin before and during isoprenaline infusion on both diets was significantly correlated (r = -0.39, n = 38, P < 0.01) with the plasma renin activity measured immediately before saralasin infusion. 4. It is concluded that during β-adrenoreceptor stimulation the increased plasma renin activity (acting through angiotensin) supports arterial pressure).