CARDIORESPIRATORY AND RENAL RESPONSES TO ARTERIAL CHEMORECEPTOR STIMULATION BY HYPOXIA OR ALMITRINE IN MEN

Citation
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
Citations number
37
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
03051870
Volume
23
Issue
12
Year of publication
1996
Pages
1021 - 1027
Database
ISI
SICI code
0305-1870(1996)23:12<1021:CARRTA>2.0.ZU;2-D
Abstract
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.