Work contained within this manuscript has previously been presented as oral abstract communication format.
Plasma Renin Activity and Aldosterone Concentrations in Hypertensive Cats with and without Azotemia and in Response to Treatment with Amlodipine Besylate
Article first published online: 13 NOV 2013
Copyright © 2013 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 28, Issue 1, pages 144–153, January/February 2014
How to Cite
Jepson, R.E., Syme, H.M. and Elliott, J. (2014), Plasma Renin Activity and Aldosterone Concentrations in Hypertensive Cats with and without Azotemia and in Response to Treatment with Amlodipine Besylate. Journal of Veterinary Internal Medicine, 28: 144–153. doi: 10.1111/jvim.12240
Syme H.M. and Elliott J., 11th ECVIM-CA/ESVIM Congress, 2001, Dublin, Ireland.
Syme H.M, Markwell P and Elliott J, 2002 ACVIM Forum, Dallas, TX, USA
- Issue published online: 15 JAN 2014
- Article first published online: 13 NOV 2013
- Manuscript Accepted: 23 SEP 2013
- Manuscript Revised: 21 AUG 2013
- Manuscript Received: 23 APR 2013
- The Waltham Centre for Pet Nutrition
- PetPlan Charitable Trust
- Blood pressure;
- Chronic kidney disease
Role of renin-angiotensin aldosterone system (RAAS) in feline systemic hypertension is poorly understood.
Examine plasma renin activity (PRA) and plasma aldosterone concentrations (PAC) in normotensive and hypertensive cats with variable renal function and in response to antihypertensive therapy.
One hundred and ninety-six cats >9 years from first opinion practice.
PRA, PAC, and aldosterone-to-renin ratio (ARR) were evaluated in cats recruited prospectively and grouped according to systolic blood pressure (SBP) and renal function (nonazotemic normotensive [Non-Azo-NT], nonazotemic hypertensive [Non-Azo-HT], azotemic normotensive [Azo-NT], azotemic hypertensive [Azo-HT]). Changes in PRA and PAC were evaluated with antihypertensive therapy (amlodipine besylate).
Plasma renin activity (ng/mL/h; P = .0013), PAC (pg/mL; P < .001), and ARR (P = 0.0062) differed significantly among groups. PRA (ng/mL/h) was significantly lower in hypertensive (Non-Azo-HT; n = 25, median 0.22 [25th percentile 0.09, 75th percentile 0.39], Azo-HT; n = 44, 0.33 [0.15, 0.48]) compared with Non-Azo-NT cats (n = 57, 0.52 [0.28, 1.02]). Azo-HT cats had significantly higher PAC (n = 22, 149.8 [103.1, 228.7]) than normotensive cats (Non-Azo-NT; n = 26, 45.4 [19.6, 65.0], Azo-NT; n = 18, 84.1 [38.6, 137.8]). ARR was significantly higher in Azo-HT (n = 20, 503.8 [298.8, 1511]) than Azo-NT cats (n = 16, 97.8 [77.0, 496.4]). Significant increase in PRA was documented with antihypertensive therapy (pretreatment [n = 20] 0.32 [0.15–0.46], posttreatment 0.54 [0.28, 1.51]), but PAC did not change.
Conclusions and Clinical Importance
Hypertensive cats demonstrate significantly increased PAC with decreased PRA. PRA significantly increases with antihypertensive therapy. Additional work is required to determine the role of plasma aldosterone concentration in the pathogenesis of hypertension and whether this relates to autonomous production or activation of RAAS without demonstrable increase in PRA.