H. Brauer et al., CARDIORESPIRATORY AND RENAL RESPONSES TO ARTERIAL CHEMORECEPTOR STIMULATION BY HYPOXIA OR ALMITRINE IN MEN, Clinical and experimental pharmacology and physiology, 23(12), 1996, pp. 1021-1027
1. The cardiorespiratory and renal responses to 3 h of normobaric whol
e-body hypoxic hypoxia (FiO2 = 0.12) as well as to arterial chemorecep
tor stimulation by the oral administration of 100 mg almitrine bismesy
late during normoxia were measured in 12 normotensive young men underg
oing water diuresis. A third series of responses obtained under compar
able conditions in the same subjects served as time controls. 2. No si
gnificant changes could be detected over time in the parameters measur
ed in control experiments. The subjects reacted to both whole-body hyp
oxic hypoxia and to pharmacological chemoreceptor stimulation with sig
nificant increases in heart rate, tidal volume, minute ventilation and
filtration fraction. Overall renal vascular resistance rose significa
ntly in hypoxia; increases in renal vascular resistance in almitrine e
xperiments were not significant, 3. Renal fractional lithium excretion
decreased significantly in response to whole-body hypoxic hypoxia and
increased slightly in response to almitrine. Fractional urine and sod
ium excretion showed negligible changes. 4. The data indicate that, in
humans, both almitrine and whole-body hypoxic hypoxia affect not only
alveolar ventilation but also renal haemodynamics. 5. The renal elect
rolyte excretion pattern suggests that under certain circumstances (e.
g, dilated renal vascular bed) acute, but well-tolerated, whole-body h
ypoxic hypoxia can simultaneously stimulate renal proximal tubular sod
ium reabsorption and inhibit distal tubular sodium reabsorption. The r
enal tubular responses also indicate that almitrine may influence rena
l tubular lithium reabsorption by, thus far, unknown mechanisms.