Characterization of the myocardial and renal renin–angiotensin system in normal cats and cats with hypertrophic cardiomyopathy

Abstract Background The tissue renin–angiotensin system (RAS) has not been characterized in cats. Hypothesis/Objectives To quantify RAS enzyme activity and angiotensin peptide (AP) concentrations in myocardial and renal tissue obtained at necropsy from healthy cats and cats with hypertrophic cardiomyopathy (HCM). Animals A convenience sample of 17 adult purpose-bred cats, euthanized under other study protocols, with echocardiographically normal hearts (n = 8) or American College of Veterinary Internal Medicine stage B1 (n = 6) or C (n = 3) HCM. Methods Prospective study. Tissues were incubated with spiked angiotensin I (AngI) or II (AngII) under control and inhibitor conditions to assess relative enzyme contributions to AngII or angiotensin 1-7 (Ang1-7) formation. Freezing was delayed for 3 h in paired samples from 7 cats. Angiotensin peptides were also directly quantified in homogenized tissues. Results Renin–angiotensin system enzyme activity was present in necropsy tissues, which formed AngII and Ang1-7 when incubated with AP precursors. The median contribution of angiotensin-converting enzyme to AngII formation exceeded 85% in all tissues. The 90% confidence limits of the geometric mean of the ratio of the angiotensin production of paired samples met the equivalence requirement in 1/13 experiments. The AP concentrations were quantifiable and did not differ between cats with echocardiographically normal hearts and cats with HCM (myocardial AngI P = .11 and AngII P = .37; kidney AngI P = .84, AngII P = .73, and Ang 1-7 P = .84). Conclusions and clinical importance Necropsy tissue RAS enzyme activity and some AP concentrations were quantifiable in this cohort. Renin–angiotensin system enzyme activity changed during a short (3 h) postmortem period.