Cats with untreated systemic arterial hypertension had lower mean serum angiotensin I, II, and III concentrations than healthy controls (e.g., Ang II 33.63 vs 124.24 pmol/L; P≤0.038).
Observational (n=40)
No
How do circulating RAAS markers compare between healthy cats and those with non-hypertensive CKD or untreated systemic arterial hypertension, and does amlodipine therapy alter these markers in hypertensive cats?
There is no evidence of circulating RAAS activation in cats with non-hypertensive CKD or untreated systemic arterial hypertension, though amlodipine therapy increases angiotensin peptides in hypertensive cats.
valor p: p=≤ .038
BACKGROUND: Information on the classical and alternative circulating renin-angiotensin-aldosterone systems (RAAS) in cats with non-hypertensive chronic kidney disease (NHT-CKD) or systemic arterial hypertension (SAH) is limited. Age and diet affect the RAAS. HYPOTHESIS/OBJECTIVES: To compare serum equilibrium concentrations of angiotensin peptides and aldosterone in healthy cats and cats with NHT-CKD or untreated SAH, and to evaluate changes in these concentrations in hypertensive cats administered amlodipine. ANIMALS: Client-owned cats with NHT-CKD (serum creatinine ≥ 1.6 mg/dL, systolic blood pressure SBP < 160 mmHg; n = 17), SAH (SBP ≥ 160 mmHg or ≥ 150 mmHg with hypertensive ocular lesions; n = 6), or normal SBP (<140 mmHg) and kidney function (n = 17). METHODS: Prospective, single-center, observational study. Cats underwent indirect SBP measurement and clinicopathologic analyses. Serum was obtained contemporaneously in all cats, and after 2-4 weeks of amlodipine therapy in hypertensive cats, for evaluation of angiotensin I, II, III, IV, 1-5, and 1-7, and aldosterone. RESULTS: Adjusting for diet, age, or both modified the conclusions of statistical comparisons for several variables. Mean serum angiotensin I, II, and III concentrations were lower in cats with untreated SAH vs healthy controls across unadjusted and diet-, age-, or both diet- and age-adjusted linear mixed models (geometric mean 95% CI angiotensin I, 9.02 3.05-26.62 vs 29.78 21.15-41.94 pmol/L; angiotensin II, 33.63 12.25-92.26 vs 124.24 90.52-170.51 pmol/L; angiotensin III, 1.56 0.88-2.79 vs 7.96 5.35-11.86 pmol/L; all P ≤ .038). Controlling for diet but not age, angiotensin II (P = .043) and III (P = .019) were also lower in cats with NHT-CKD vs controls. All angiotensin peptides, except for angiotensin IV, significantly increased in hypertensive cats during amlodipine therapy. Serum aldosterone did not differ between groups, or before and after amlodipine in hypertensive cats. CONCLUSIONS AND CLINICAL IMPORTANCE: Evidence of circulating RAAS activation in cats with NHT-CKD or untreated SAH was not found.
Lourenço et al. (Fri,) conducted a observational in non-hypertensive chronic kidney disease or systemic arterial hypertension (n=40). amlodipine vs. healthy controls was evaluated on serum equilibrium concentrations of angiotensin peptides and aldosterone (p=≤ .038). Cats with untreated systemic arterial hypertension had lower mean serum angiotensin I, II, and III concentrations than healthy controls (e.g., Ang II 33.63 vs 124.24 pmol/L; P≤0.038).