Twenty-four hour pressor effect of infused adrenaline in normotensive subjects: A randomized controlled double-blind cross-over study

Stimulation of prejunctional β₂-adrenoceptors on sympathetic nerve terminals increases vasoconstrictor nerve activity by facilitating release of noradrenaline. Therefore, man’s endogenous β₂-adrenoceptor agonist adrenaline has been implicated in the pathogenesis of hypertension. To test this hypothesis, adrenaline (15ng/kg per min), noradrenaline (30 ng/kg per min) and saline (0.9% NaCI, 5.4 ml/h) were infused in 10 supine, resting healthy volunteers for 6 h (1000-1600 h) in random order 2 weeks apart in a double-blind crossover fashion. During infusion of noradrenaline and adrenaline, venous plasma concentrations rose to 705 ± 58 (mean ± s.e.m) and 230 ± 28 pg/ml, respectively. Mean arterial pressure rose by 4% (P < 0.001) during noradrenaline and fell by 5% (P < 0.001) during the adrenaline infusion compared with the saline infusion. In the postinfusion period (1600-0900 h) mean arterial pressure was 7% higher (P < 0.01) after adrenaline compared with the saline infusion, whereas after the noradrenaline infusion, values of mean arterial pressure were not different from those during the saline infusion. The pressor effect of adrenaline could not be explained by a central mechanism or by activation of the renin-angiotensin system. Thus, ‘stress levels’ of adrenaline mediate a delayed and protracted pressor effect. This is most likely due to stimulation of prejunctional β₂-adrenoceptors, since ‘stress levels’ of noradrenaline are devoid of such activity. Our data support the ‘adrenaline-hypertension’ hypothesis in man.