ArticleJournal of veterinary internal medicine2021
Effect of spironolactone and benazepril on furosemide-induced diuresis and renin-angiotensin-aldosterone system activation in normal dogs.
Article in Journal of veterinary internal medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- [Effects and Efficacy of Wenyang Huayin Yangxin Prescription on the Traditional Chinese Medicine Syndromes of Patients With Chronic Heart Failure Combined With Diuretic Resistance].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Trial
- Sodium-glucose cotransporter 2 inhibitors for hypertension in cardiovascular-kidney-metabolic syndrome.Experimental physiology · 2025Review
- Retrospective evaluation of risk factors for development of kidney injury after parenteral furosemide treatment of left-sided congestive heart failure in dogs.Journal of veterinary internal medicine · 2022Article
- Effect of spironolactone and benazepril on furosemide-induced diuresis and renin-angiotensin-aldosterone system activation in normal dogs.Journal of veterinary internal medicine · 2021Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDiuretic braking during furosemide continuous rate infusion (FCRI) curtails urine production. HYPOTHESIS: Renin-angiotensin-aldosterone system (RAAS) activation mediates braking, and RAAS inhibition will increase urine production. ANIMALS: Ten healthy purpose-bred male dogs.
methodsDogs 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.
resultsDiuretic 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.
conclusionsThe 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.
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