Effect of spironolactone and benazepril on furosemide-induced diuresis and renin-angiotensin-aldosterone system activation in normal dogs.
aldosterone antagonist
angiotensin-converting enzyme inhibitor
continuous rate infusion
diuretic resistance
neurohormone
urine production
Journal
Journal of veterinary internal medicine
ISSN: 1939-1676
Titre abrégé: J Vet Intern Med
Pays: United States
ID NLM: 8708660
Informations de publication
Date de publication:
May 2021
May 2021
Historique:
revised:
15
02
2021
received:
22
09
2020
accepted:
19
02
2021
pubmed:
14
3
2021
medline:
29
6
2021
entrez:
13
3
2021
Statut:
ppublish
Résumé
Diuretic braking during furosemide continuous rate infusion (FCRI) curtails urine production. Renin-angiotensin-aldosterone system (RAAS) activation mediates braking, and RAAS inhibition will increase urine production. Ten healthy purpose-bred male dogs. Dogs received placebo, benazepril, or benazepril and spironolactone PO for 3 days before a 5-hour FCRI (0.66 mg/kg/h) in a 3-way, randomized, blinded, cross-over design. Body weight (BW), serum creatinine concentration (sCr), serum electrolyte concentrations, PCV, and total protein concentration were measured before PO medications, at hours 0 and 5 of FCRI, and at hour 24. During the FCRI, water intake, urine output, urine creatinine concentration, and urine electrolyte concentrations were measured hourly. Selected RAAS components were measured before and after FCRI. Variables were compared among time points and treatments. Diuretic braking and urine production were not different among treatments. Loss of BW, hemoconcentration, and decreased serum chloride concentration occurred during FCRI with incomplete recovery at hour 24 for all treatments. Although unchanged during FCRI, sCr increased and serum sodium concentration decreased at hour 24 for all treatments. Plasma aldosterone and angiotensin-II concentrations increased significantly at hour 5 for all treatments, despite suppressed angiotensin-converting enzyme activity during benazepril background treatment. The neurohormonal profile during FCRI supports RAAS mediation of diuretic braking in this model. Background treatment with benazepril with or without spironolactone did not mitigate braking, but was well tolerated. Delayed changes in sCr and serum sodium concentration and incomplete recovery of hydration indicators caused by furosemide hold implications for clinical patients.
Sections du résumé
BACKGROUND
BACKGROUND
Diuretic braking during furosemide continuous rate infusion (FCRI) curtails urine production.
HYPOTHESIS
OBJECTIVE
Renin-angiotensin-aldosterone system (RAAS) activation mediates braking, and RAAS inhibition will increase urine production.
ANIMALS
METHODS
Ten healthy purpose-bred male dogs.
METHODS
METHODS
Dogs received placebo, benazepril, or benazepril and spironolactone PO for 3 days before a 5-hour FCRI (0.66 mg/kg/h) in a 3-way, randomized, blinded, cross-over design. Body weight (BW), serum creatinine concentration (sCr), serum electrolyte concentrations, PCV, and total protein concentration were measured before PO medications, at hours 0 and 5 of FCRI, and at hour 24. During the FCRI, water intake, urine output, urine creatinine concentration, and urine electrolyte concentrations were measured hourly. Selected RAAS components were measured before and after FCRI. Variables were compared among time points and treatments.
RESULTS
RESULTS
Diuretic braking and urine production were not different among treatments. Loss of BW, hemoconcentration, and decreased serum chloride concentration occurred during FCRI with incomplete recovery at hour 24 for all treatments. Although unchanged during FCRI, sCr increased and serum sodium concentration decreased at hour 24 for all treatments. Plasma aldosterone and angiotensin-II concentrations increased significantly at hour 5 for all treatments, despite suppressed angiotensin-converting enzyme activity during benazepril background treatment.
CONCLUSIONS
CONCLUSIONS
The neurohormonal profile during FCRI supports RAAS mediation of diuretic braking in this model. Background treatment with benazepril with or without spironolactone did not mitigate braking, but was well tolerated. Delayed changes in sCr and serum sodium concentration and incomplete recovery of hydration indicators caused by furosemide hold implications for clinical patients.
Identifiants
pubmed: 33713485
doi: 10.1111/jvim.16097
pmc: PMC8163123
doi:
Substances chimiques
Angiotensin-Converting Enzyme Inhibitors
0
Benzazepines
0
Diuretics
0
Spironolactone
27O7W4T232
Aldosterone
4964P6T9RB
Furosemide
7LXU5N7ZO5
benazepril
UDM7Q7QWP8
Types de publication
Journal Article
Randomized Controlled Trial, Veterinary
Langues
eng
Sous-ensembles de citation
IM
Pagination
1245-1254Subventions
Organisme : Ceva Santé Animale
Informations de copyright
© 2021 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.
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