Key result
IV furosemide increases RAAS peptides in healthy horses, raising AngII by ~34 pmol/L at 4 hours.
Why the study?
Furosemide activates the renin-angiotensin-aldosterone system in other species, but little is known about RAAS peptide activation in horses.
Does a single dose of furosemide cause transient increases in renin-angiotensin-aldosterone system (RAAS) peptides in healthy horses?
RCT (n=14)
Open-label
Randomly allocated into 2 groups
No
Does a single dose of furosemide cause transient increases in renin-angiotensin-aldosterone system (RAAS) peptides in healthy horses?
Mean Difference: 33.7 (95% CI 9.6–57.9)
p-value: p=0.0008
A single dose of furosemide in healthy horses causes a transient increase in both classical and alternative RAAS pathway hormones, which can be reliably measured using serum equilibrium analysis.
Furosemide transiently activates RAAS peptides in healthy horses; leaves open relevance to clinical equine disease or therapeutic implications.
BACKGROUND: Furosemide, a commonly used diuretic, activates the renin-angiotensin-aldosterone system (RAAS) in other species. Little is known about RAAS peptide activation in horses. HYPOTHESIS/OBJECTIVES: To evaluate equilibrium analysis as a practical method for RAAS quantification in horses and describe the RAAS response to a single dose of furosemide. We hypothesize that furosemide would cause transient increase in RAAS peptides in horses. ANIMALS: 14 healthy adult thoroughbreds from a university teaching herd. METHODS: Horses received either furosemide (1 mg/kg IV) or saline IV in a crossover study design. Protease-inhibited samples were compared with equilibrium analysis samples with Deming regression analysis. Renin-angiotensin-aldosterone system hormones were evaluated at 0, 0.25, 0.5, 4, and 24 hours postadministration, via equilibrium analysis. Values were compared with a mixed effects model. RESULTS: Correlation between protease inhibition and equilibrium analysis was high for angiotensin I peptide (AngI) and angiotensin II peptide (AngII) (r = .92 and .95, respectively). Baseline RAAS peptide concentrations were below the limit of detection except AngII (median, 7.5 [range, 3.5-14.0] pmol/L). Furosemide administration resulted in an increase in AngI (8.0 [0.5-15.5] pmol/L, P = .03), AngII (33.7 [9.6-57.9] pmol/L, P = .0008), angiotensin III peptide (AngIII) (2.9 [0.9-4.9] pmol/L, P = .0005), angiotensin IV peptide (AngIV) (2.0 [0.6-3.4] pmol/L, P = .0005), and angiotensin 1-5 peptide (Ang1-5) (5.6 [1.2-5.9] pmol/L, P = .003) at 4 hours. Differences are reported as difference in the mean (95% confidence interval [CI]). CONCLUSIONS AND CLINICAL IMPORTANCE: Furosemide produced an increase in hormones associated with both the classical and alternative RAAS pathways. Serum equilibrium analysis is practical for RAAS analysis in horses.
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Lehman et al. (2024) conducted an RCT in Healthy (Veterinary) (n=14). Furosemide vs. Saline IV (0.9%) was evaluated on Angiotensin II peptide (AngII) concentration difference between groups at 4 hours post-administration (MD 33.7 pmol/L, 95% CI 9.6-57.9, p=0.0008). A single intravenous dose of furosemide in healthy Thoroughbred horses significantly increased both classical and alternative renin-angiotensin-aldosterone system peptides, including AngII by a mean difference of 33.7 pmol/L at 4 hours.
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