Background: The local (tissue) renin-angiotensin system (RAS) has not been characterized in cats. Hypothesis/
Objectives: Investigate myocardial and renal tissue RAS regulation in cardiovascularly healthy and hypertrophic cardiomyopathy (HCM) affected cats. Animals: A convenience sample of 17 adult purpose-bred cats euthanized for other study protocols and confirmed to be healthy (n=8); ACVIM stage B1 HCM (n=6); and ACVIM Stage C HCM (n=3). Cats were not receiving any medications.
Methods: Left ventricular myocardium and renal cortex and medulla samples were harvested and immediately flash frozen within 10 minutes of euthanasia, with a second sample held at room temperature for three hours prior to freezing. Mass spectrometry was used to quantify serum and tissue angiotensin peptide (AP) concentrations and to estimate select RAS enzyme activities. Tissue AP concentrations were compared between groups using Kruskal-Wallis analysis. Angiotensin (Ang) II and 1,7 formation rates in fresh and 3-hour samples were compared using Bland-Altman analysis.
Results: Angiotensin I and II were the only measurable APs in the myocardial samples. Angiotensin I, II, and 1,7 were measurable in all kidney samples. Myocardial and renal AP concentrations did not differ among the groups (AngII: p=0.32 and p=0.68 for myocardium and kidney, respectively). Endogenous angiotensin-converting enzyme, not chymase, was the greatest contributor to AngII formation in both tissues, regardless of disease status. The AP formation rates assay was stable in the 3-hour samples. Conclusions and clinical importance: Tissue RAS was not activated by advanced HCM in this cohort. RAS enzyme activity is stable for at least three hours postmortem.
