Renal and neurohormonal responses to increasing levels of lower body negative pressure in men.

Détails

ID Serval
serval:BIB_619256814E32
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Renal and neurohormonal responses to increasing levels of lower body negative pressure in men.
Périodique
Kidney international
Auteur(s)
Würzner G., Chiolero A., Maillard M., Nussberger J., Hayoz D., Brunner H.R., Burnier M.
ISSN
0085-2538
Statut éditorial
Publié
Date de publication
2001
Peer-reviewed
Oui
Volume
60
Numéro
4
Pages
1469-76
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't - Publication Status: ppublish
Résumé
BACKGROUND: The stimulation of efferent renal sympathetic nerve activity induces sequential changes in renin secretion, sodium excretion, and renal hemodynamics that are proportional to the magnitude of the stimulation of sympathetic nerves. This study in men investigated the sequence of the changes in proximal and distal renal sodium handling, renal and systemic hemodynamics, as well as the hormonal profile occurring during a sustained activation of the sympathetic nervous system induced by various levels of lower body negative pressure (LBNP). METHODS: Ten healthy subjects were submitted to three levels of LBNP ranging between 0 and -22.5 mm Hg for one hour according to a triple crossover design, with a minimum of five days between each level of LBNP. Systemic and renal hemodynamics, renal water and sodium handling (using the endogenous lithium clearance technique), and the neurohormonal profile were measured before, during, and after LBNP. RESULTS: LBNP (0 to -22.5 mm Hg) induced an important hormonal response characterized by a significant stimulation of the sympathetic nervous system and gradual activations of the vasopressin and the renin-angiotensin systems. LBNP also gradually reduced water excretion and increased urinary osmolality. A significant decrease in sodium excretion was apparent only at -22.5 mm Hg. It was independent of any change in the glomerular filtration rate and was mediated essentially by an increased sodium reabsorption in the proximal tubule (a significant decrease in lithium clearance, P < 0.05). No significant change in renal hemodynamics was found at the tested levels of LBNP. As observed experimentally, there appeared to be a clear sequence of responses to LBNP, the neurohormonal response occurring before the changes in water and sodium excretion, these latter preceding any change in renal hemodynamics. CONCLUSIONS: These data show that the renal sodium retention developing during LBNP, and thus sympathetic nervous stimulation, is due mainly to an increase in sodium reabsorption by the proximal segments of the nephron. Our results in humans also confirm that, depending on its magnitude, LBNP leads to a step-by-step activation of neurohormonal, renal tubular, and renal hemodynamic responses.
Mots-clé
Adult, Cross-Over Studies, Hemodynamics, Humans, Kidney, Kidney Tubules, Lower Body Negative Pressure, Male, Neurotransmitter Agents, Renal Circulation, Sodium
Pubmed
Web of science
Open Access
Oui
Création de la notice
17/01/2008 17:38
Dernière modification de la notice
20/08/2019 15:18
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