OBJECTIVES The mechanism of hypertension in Gushing's syndrome remains unde
termined, Some studies have demonstrated an increased sensitivity to presse
r agents but it is not clear if patients with Gushing's syndrome of differe
nt aetiologies demonstrate this finding. We have examined presser sensitivi
ty in a group of patients with Gushing's disease (pituitary dependent hyper
cortisolism) by measuring blood pressure during incrementally increasing in
fusions of noradrenaline.
METHODS Eight subjects (7 female, 1 male), aged 42.2 +/- 4.5 years (mean +/
- SEM) with Gushing's disease were studied, Eight age- and sex-matched cont
rol subjects were also studied. Four of the eight controls and five patient
s with Gushing's disease had elevated blood pressure, All medication for th
is had been stopped at least seven days prior to the study, After subjects
ate a light breakfast, EGG leads and a sphygmomanometer were attached, an i
ntravenous cannula was inserted and all subjects then rested quietly for 60
minutes, Noradrenaline was then infused intravenously for 10-minute period
s at concentrations of 0.01, 0.03, 0.07, 0.11 and 0.18 mu g/kg/minute.
RESULTS On the day of the study the baseline blood pressures and pulse rate
s in the patients with Cushing's disease (blood pressure; 138/87 +/- 6/3mmH
g, pulse 76.5 +/- 4.8 beats/minute) and controls (blood pressure; 126/86 +/
- 6/6 mmHg, pulse 71.2 +/- 3.7 beats/ minute) were not significantly differ
ent. The mean change in diastolic blood pressure from baseline at the time
of the peak increase or when the test was stopped was 21.5 +/- 4.7 mmHg in
Gushing's disease compared to 7.0 +/- 2.5 mmHg in controls (P = 0.03). The
mean change in mean arterial pressure from baseline at the time of the peak
increase or when the test was stopped was 22.0 +/- 4.0 mmHg in Gushing's d
isease compared to 13.0 +/- 2.4 mmHg in controls (P = 0.03). No significant
difference in mean change of systolic pressure (26.0 +/- 4.6 vs.25 +/- 4.0
mmHg) or pulse rates (- 11.1 +/- 1 8 vs, - 4.7 +/- 2.6) was seen in the gr
oup with Gushing's disease as compared to the control group,
CONCLUSIONS We conclude that patients with pituitary-dependent Gushing's sy
ndrome have enhanced presser diastolic and mean arterial responses to norad
renaline and this may be an important underlying mechanism for the hyperten
sion seen in this particular group of Gushing's syndrome patients.