Angiotensin II receptor blockade prevents acute renal sodium retention induced by low levels of orthostatic stress.

Détails

ID Serval
serval:BIB_0ECD16DDBFAE
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Angiotensin II receptor blockade prevents acute renal sodium retention induced by low levels of orthostatic stress.
Périodique
Kidney International
Auteur(s)
Wuerzner G., Chioléro A., Maillard M., Nussberger J., Brunner H.R., Burnier M., Chiclero A.
ISSN
0085-2538 (Print)
ISSN-L
0085-2538
Statut éditorial
Publié
Date de publication
2004
Peer-reviewed
Oui
Volume
65
Numéro
1
Pages
238-244
Langue
anglais
Notes
Publication types: Clinical Trial ; Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
BACKGROUND: Depending on its magnitude, lower body negative pressure (LBNP) has been shown to induce a progressive activation of neurohormonal, renal tubular, and renal hemodynamic responses, thereby mimicking the renal responses observed in clinical conditions characterized by a low effective arterial volume such as congestive heart failure. Our objective was to evaluate the impact of angiotensin II receptor blockade with candesartan on the renal hemodynamic and urinary excretory responses to a progressive orthostatic stress in normal subjects.
METHODS: Twenty healthy men were submitted to three levels of LBNP (0, -10, and -20 mbar or 0, -7.5, and -15 mm Hg) for 1 hour according to a crossover design with a minimum of 2 days between each level of LBNP. Ten subjects were randomly allocated to receive a placebo and ten others were treated with candesartan 16 mg orally for 10 days before and during the three levels of LBNP. Systemic and renal hemodynamics, renal sodium excretions, and the hormonal response were measured hourly before, during, and for 2 hours after LBNP.
RESULTS: During placebo, LBNP induced no change in systemic and renal hemodynamics, but sodium excretion decreased dose dependently with higher levels of LBNP. At -20 mbar, cumulative 3-hour sodium balance was negative at -2.3 +/- 2.3 mmol (mean +/- SEM). With candesartan, mean blood pressure decreased (76 +/- 1 mm Hg vs. 83 +/- 3 mm Hg, candesartan vs. placebo, P < 0.05) and renal plasma flow increased (858 +/- 52 mL/min vs. 639 +/- 36 mL/min, candesartan vs. placebo, P < 0.05). Glomerular filtration rate (GFR) was not significantly higher with candesartan (127 +/- 7 mL/min in placebo vs. 144 +/- 12 mL/min in candesartan). No significant decrease in sodium and water excretion was found during LBNP in candesartan-treated subjects. At -20 mbar, the 3-hour cumulative sodium excretion was + 4.6 +/- 1.4 mmol in the candesartan group (P= 0.02 vs. placebo).
CONCLUSION: Selective blockade of angiotensin II type 1 (AT1) receptors with candesartan increases renal blood flow and prevents the antinatriuresis during sustained lower body negative pressure despite a modest decrease in blood pressure. These results thus provide interesting insights into potential benefits of AT1 receptor blockade in sodium-retaining states such as congestive heart failure.
Mots-clé
Acute Disease, Adult, Angiotensin II/antagonists & inhibitors, Antihypertensive Agents/administration & dosage, Benzimidazoles/administration & dosage, Blood Pressure/drug effects, Cross-Over Studies, Heart Rate/drug effects, Humans, Hypotension, Orthostatic/drug therapy, Hypotension, Orthostatic/metabolism, Kidney Tubules/drug effects, Kidney Tubules/metabolism, Lower Body Negative Pressure, Male, Natriuresis/drug effects, Sodium/metabolism, Tetrazoles/administration & dosage
Pubmed
Web of science
Open Access
Oui
Création de la notice
05/03/2008 17:40
Dernière modification de la notice
20/08/2019 13:35
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