Furosemide stimulation of parathormone in humans: role of the calcium-sensing receptor and the renin-angiotensin system.

Détails

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Etat: Public
Version: Author's accepted manuscript
ID Serval
serval:BIB_A227854F597B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Furosemide stimulation of parathormone in humans: role of the calcium-sensing receptor and the renin-angiotensin system.
Périodique
Pflugers Archiv
Auteur(s)
Muller M.E., Forni Ogna V., Maillard M., Stoudmann C., Zweiacker C., Anex C., Wuerzner G., Burnier M., Bonny O.
ISSN
1432-2013 (Electronic)
ISSN-L
0031-6768
Statut éditorial
Publié
Date de publication
12/2015
Peer-reviewed
Oui
Volume
467
Numéro
12
Pages
2413-2421
Langue
anglais
Notes
Publication types: Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Interactions between sodium and calcium regulating systems are poorly characterized but clinically important. Parathyroid hormone (PTH) levels are increased shortly after furosemide treatment by an unknown mechanism, and this effect is blunted by the previous administration of a calcimimetic in animal studies. Here, we explored further the possible underlying mechanisms of this observation in a randomized crossover placebo-controlled study performed in 18 human males. Volunteers took either cinacalcet (60 mg) or placebo and received a 20 mg furosemide injection 3 h later. Plasma samples were collected at 15-min intervals and analyzed for intact PTH, calcium, sodium, potassium, magnesium, phosphate, plasma renin activity (PRA), and aldosterone up to 6 h after furosemide injection. Urinary electrolyte excretion was also monitored. Subjects under placebo presented a sharp increase in PTH levels after furosemide injection. In the presence of cinacalcet, PTH levels were suppressed and marginal increase of PTH was observed. No significant changes in electrolytes and urinary excretion were identified that could explain the furosemide-induced increase in PTH levels. PRA and aldosterone were stimulated by furosemide injection but were not affected by previous cinacalcet ingestion. Expression of NKCC1, but not NKCC2, was found in parathyroid tissue. In conclusion, our results indicate that furosemide acutely stimulates PTH secretion in the absence of any detectable electrolyte changes in healthy adults. A possible direct effect of furosemide on parathyroid gland needs further studies.

Mots-clé
Adolescent, Adult, Aldosterone/blood, Calcimimetic Agents/pharmacology, Calcium/blood, Cinacalcet Hydrochloride/pharmacology, Diuretics/administration & dosage, Diuretics/pharmacology, Female, Furosemide/administration & dosage, Furosemide/pharmacology, Humans, Male, Middle Aged, Parathyroid Glands/metabolism, Parathyroid Hormone/blood, Receptors, Calcium-Sensing/metabolism, Renin/blood, Renin-Angiotensin System/drug effects, Solute Carrier Family 12, Member 1/genetics, Solute Carrier Family 12, Member 1/metabolism, Solute Carrier Family 12, Member 2/genetics, Solute Carrier Family 12, Member 2/metabolism, Calcium-sensing receptor, Cinacalcet, Furosemide, Mineral metabolism, Renin-angiotensin-aldosterone system
Pubmed
Web of science
Open Access
Oui
Création de la notice
07/10/2015 16:30
Dernière modification de la notice
20/08/2019 15:08
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