Traffic in Humans

Background. Adenosine is an effective hypotensive agent in experimental animals and in anesthetized patients, producing little if any evidence of reflex sympathetic activation. In contrast, adenosine increases systolic blood pressure and heart rate in conscious subjects. To determine whether this response is related to sympathetic activation, we studied the cardiovascular and respiratory effects of adenosine in normal subjects while measuring muscle sympathetic nerve traffic through direct recordings from a peroneal nerve. Methods and Results. Adenosine (80 ,ug/kg/min i.v.) increased heart rate (+32±3 beats/min), systolic blood pressure (+10±2 mm Hg), and minute ventilation (+7±1 1/min). This was accompanied by a dose-dependent increase in muscle sympathetic nerve activity (from 198±52 to 451±92 units/min). Adenosine also produced a small, but consistent, decrease in diastolic blood pressure (-6±3 mm Hg). Adenosine produced a greater increase in sympathetic nerve traffic (145±32% above baseline) than did nitroprusside (65±16%) at doses that resulted in equivalent decreases in diastolic blood pressure. Arterial baroreceptor unloading, therefore, could not totally explain the increase in sympathetic traffic produced by adenosine. Conclusions. Given the constellation of findings of increased ventilation and sympathetic activity, we, therefore, propose that adenosine increases sympathetic tone by activating afferent nerves, including arterial chemoreceptors. Contrary to the known inhibitory actions of adenosine on central and peripheral efferent systems, this and other reports suggest that adenosine-induced activation of afferent nerves, leading to sympathetic activation, may be a more widespread phenomenon than previously recognized. (Circulation 1991;83:1668-1675)