thesis
Adrenaline and hypertension
- Publication date
- 2 October 1991
- Publisher
- 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?