HUMAN MUSCLE SYMPATHETIC ACTIVITY AND CARDIAC CATECHOLAMINE SPILLOVER- NO SUPPORT FOR AUGMENTED SYMPATHETIC NORADRENALINE RELEASE BY ADRENALINE COTRANSMISSION

1. Evidence from animal studies indicates that circulating adrenaline may be taken up into sympathetic nerves, facilitating the release of n oradrenaline. To test whether adrenaline acts as a co-transmitter in h umans we studied eight healthy men (aged 19-23 years) during isometric handgrip before and after an adrenaline infusion (1-3 mu g/min for >3 0min). Sympathetic activity was assessed using radiotracer kinetic tec hniques to measure total and cardiac spillovers of noradrenaline and a drenaline, and microneurography to measure muscle sympathetic activity 2. During the adrenaline infusion systolic blood pressure and heart r ate increased significantly and diastolic blood pressure decreased. To tal noradrenaline spillover, and arterial and coronary sinus plasma no radrenaline concentrations, increased significantly. Muscle sympatheti c nerve traffic increased both during and after the end of the infusio n. 3. Thirty minutes after the end of the adrenaline infusion there wa s adrenaline release from the heart (1.5 +/- 0.4 ng/min. mean +/- S.E. M.) indicating that significant adrenaline loading of cardiac sympathe tic nerves had occurred. At this time muscle sympathetic nerve traffic and total body and cardiac noradrenaline spillovers were similar (P > 0.05) to pre-adrenaline infusion values (nerve traffic 24 +/- 4 versu s 21 +/- 3 bursts/min; total noradrenaline spillover 698 +/- 98 versus 618 +/- 119 ng/min; cardiac noradrenaline spillover 16.2 +/- 2.8 vers us 13.9 +/- 3.9 ng/min). 4. Isometric handgrip contraction evoked simi lar responses pre-and post-adrenaline infusion in total and cardiac no radrenaline spillovers and in muscle sympathetic activity. 5. The resu lts do not support the theory that adrenaline is a co-transmitter faci litating noradrenaline release from human sympathetic nerves.