Targeted proteomic analyses during combined angiotensin-converting enzyme inhibitor and mineralocorticoid receptor antagonist administration (CARDALIS®) in healthy dogs.

Benazepril/spironolactone combination therapy upregulates cardioprotective and anti-inflammatory plasma proteins in RAAS-activated healthy dogs.

This prospective experimental study investigated the proteomic effects of renin-angiotensin-aldosterone system (RAAS) activation and subsequent inhibition using a benazepril/spironolactone combination (CARDALIS®) in 18 healthy beagle dogs. Dogs were placed on a low-sodium diet to induce RAAS activation, then randomized to one of three dosing regimens for 14 days: label dose (benazepril 0.25 mg/kg + spironolactone 2 mg/kg q24h), intermediate dose (same drugs q12h), or high dose (benazepril 0.5 mg/kg + spironolactone 4 mg/kg q12h). Using Olink proximity extension assay technology, 177 plasma proteins were quantified across the Inflammation and Cardiovascular II panels. RAAS activation induced by low-sodium diet was associated with downregulation of cardioprotective proteins (ACE2, FGF-5), adaptive immune mediators (CCL4), and tissue repair markers (MMP-10). Treatment with benazepril/spironolactone reversed several of these changes, upregulating ACE2 and adaptive immune proteins such as CCL4 and TSLP. Some biomarker responses showed dose-dependent differences. These findings suggest that combination RAAS inhibition exerts measurable anti-inflammatory and anti-fibrotic effects at the proteomic level in dogs, potentially relevant to management of cardiac diseases such as myxomatous mitral valve disease. Limitations include the use of healthy dogs rather than naturally diseased patients and the short treatment duration. This study provides foundational proteomic data to guide future investigations in dogs with naturally occurring cardiovascular disease.

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