Adrenaline and hypertension

The questions we hoped to answer by the studies described in this thesis, were: 1 Does adrenaline, when infused intravenously in normotensive subjects leading to plasma levels in the high physiological range, cause a sustained and protracted rise in blood pressure, which outlasts the duration of the increments in circulating adrenaline? And if so, does this effect on blood pressure occurs at rest or during periods of activation of the sympathetic nervous system? In view of the data of Vincent et al (43), we hypothesized that the latter would be the case. 2 If the questions under number 1 are positively answered, does intravenous administered noradrenaline have the same effect? When the effect of adrenaline is indeed mediated through prejunctional B,-adrenoceptors, we hypothesized that this would not be the case. 3 Do the pressor responses to standardized sympathetic nervous system stimulation by cold pressor and isometric exercise testing before, during and 18 hours after cessation of infusions of adrenaline, noradrenaline or dextrose 5% differ? Again we hypothesized that infusion of adrenaline but not noradrenaline would lead to an amplification of the blood pressure responses. 4 Are the changes in plasma concentrations of adrenaline and noradrenaline during the infusions of adrenaline and noradrenaline also detectable in alterations in the amounts of catecholamines and their metabolites excreted in the urine? 5 Do the infusions of catechOiamines, which lead to alterations in plasma concentrations within the physiological range, have any effect on urinary sodium excretion or on plasma levels of several hormones, potassium or glucose? 6 What is the effect of non-selective and B,-selective B-blockade on the adrenaline mediated facilitation of noradrenaline release and the adrenaline induced enhancement of reflex sympathetic nervous system activity?