There is a complex interaction between pulmonary haemodynamics, hormonal, a
nd salt and water balance in patients with chronic obstructive pulmonary di
sease (COPD) and in normal subjects exposed to hypoxia or high altitude. Th
is study aims to investigate the effects of hypoxia on renal hormonal balan
ce in normal subjects and patients with CORD, particularly the role of urin
ary dopamine and atrial natriuretic peptide (ANP).
Urinary dopamine output, ANP, and plasma renin activity (PRA) were measured
in 12 normal subjects exposed to hypoxia (12% O-2) and hyperoxia (40% O-2)
for 1 h and in 15 patients with exacerbations of COPD while breathing air
or O-2. These measurements were repealed in six of the patients with exacer
bations of COPD when they were clinically stable.
Hypoxia caused an increase in ANP levels (49 +/- 6-62 +/- 6 pg ml(-1), P<0.
05) and a fall in urinary dopamine output (277 +/- 39-205 +/- 33 ng h(-1),
P<0.002) in normal subjects. Hyperoxia was associated with a return of plas
ma ANP to the baseline values. In patients with exacerbations of COPD plasm
a ANP levels were higher (181 +/- 36 pg ml(-1)) than in normal subjects (49
.5 +/- 6.5 pg ml(-1), P<0.001). Urinary dopamine output breathing air (175
+/- 34 ng h(-1)) was similar to the levels when normal subjects were made h
ypoxaemic and PRA was elevated in comparison to normal values. There was no
change in their levels following the acute administration of oxygen in pat
ients presenting with exacerbations of COPD, but oxygen improved urinary so
dium excretion (P<0.05). In six patients re-studied when clinically stable
there was a fall in urinary dopamine output, plasma ANP and PRA when breath
ing air in comparison to the acute stage of the disease (P<0.05).
These data suggest presence of renal hormonal imbalance including endogenou
s urinary dopamine output during hypoxic exacerbation of COPD and in normal
subjects exposed to hypoxia.