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Circulating renin-angiotensin-aldosterone system activity in cats with systemic hypertension or cardiomyopathy
Jessica L Ward1, Emilie Guillot2, Oliver Domenig3
1Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, Iowa, USA.
Insights
Cats with cardiomyopathy (CM) show increased renin-angiotensin-aldosterone system (RAAS) activity, while those with untreated systemic hypertension (SH) do not. Both furosemide and amlodipine treatments nonspecifically activate RAAS pathways in cats.
Area of Science:
- Veterinary Cardiology
- Endocrinology
- Pharmacology
Background:
- Circulating renin-angiotensin-aldosterone system (RAAS) activity is not well-characterized in cats with systemic hypertension (SH) or cardiomyopathy (CM).
- The impact of furosemide and amlodipine on RAAS in cats requires further investigation.
Purpose of the Study:
- To quantify RAAS activity in cats with SH or CM compared to healthy controls.
- To assess changes in RAAS profiles following furosemide or amlodipine treatment.
Main Methods:
- Serum samples from 66 cats (15 SH, 17 CM, 34 healthy) were analyzed.
- Liquid chromatography-mass spectrometry quantified RAAS peptides and aldosterone.
- Statistical analysis included Kruskal-Wallis and Dunn's tests.
Main Results:
- Cats with CM exhibited significantly higher angiotensin I, aldosterone, and plasma renin activity compared to healthy cats.
- Amlodipine-treated cats with SH showed elevated RAAS biomarkers, unlike untreated SH cats.
- Furosemide and amlodipine were independent predictors of increased RAAS biomarker concentrations.
Conclusions:
- Cardiomyopathy in cats is associated with heightened RAAS activity.
- Untreated systemic hypertension in cats does not correlate with increased RAAS activity.
- Furosemide and amlodipine induce non-specific activation of RAAS pathways in feline subjects.
Background:
Activity of the circulating renin-angiotensin-aldosterone system (RAAS) has not been comprehensively characterized in cats with systemic hypertension (SH) or cardiomyopathy (CM), and the effects of furosemide or amlodipine treatment on the RAAS have not been fully evaluated in cats.
Hypothesis/Objectives:
To document RAAS activity in cats with SH or CM compared to healthy cats and determine how RAAS profiles change with furosemide or amlodipine treatment.
Animals:
Sixty-six client-owned cats: 15 with SH (7 amlodipine-treated, 8 untreated), 17 with advanced CM (7 furosemide-treated, 10 not furosemide-treated), and 34 healthy cats.
Methods:
Equilibrium concentrations of RAAS peptides and aldosterone were quantified in serum samples by liquid chromatography-mass spectrometry. Variables were compared between groups using Kruskal-Wallis analysis with post hoc Holms-corrected Dunn's testing.
Results:
Compared with healthy cats, cats with CM had higher concentrations of angiotensin I, aldosterone, and plasma renin activity (all P < .01), and these differences remained significant (P < .03) after considering subgroups of untreated or furosemide-treated cats. Compared with healthy cats, untreated cats with SH showed no differences in RAAS biomarkers, whereas amlodipine-treated cats had higher concentrations of angiotensins I, II, III, IV, and 1-7, aldosterone, and plasma renin activity (all P < .03). Multivariable analysis determined that furosemide and amlodipine treatments were independent predictors of increased RAAS biomarker concentrations.
Conclusions And Clinical Importance:
Cats with CM had increased RAAS activity, whereas cats with untreated SH did not. Furosemide and amlodipine both led to nonspecific activation of both classical and alternative RAAS pathways in cats.
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