Abstract
Hypertension is a common problem in older cats, particularly associated with chronic kidney disease (CKD). Reduced activity of 11beta-hydroxysteroid dehydrogenase type 2 predisposes to hypertension in human patients by allowing excessive stimulation of the mineralocorticoid receptor by cortisol. This study was designed to test the hypothesis that reduced conversion of cortisol to cortisone contributes to the development of systemic hypertension in some cats with CKD and idiopathic hypertension (iHT). The study included 60 client-owned cats: 21 clinically normal, 16 normotensive cats with CKD (NTCKD), 14 hypertensive cats with CKD (HTCKD) and nine iHTs. Urine cortisol and cortisone were extracted into dichloromethane and chloroform, respectively, prior to analysis by radioimmunoassay. Data are reported as median and range. The Kruskall-Wallis test was used to compare cortisol:cortisone ratios between groups with post-hoc testing using the Mann-Whitney U test. Wilcoxon signed-ranks test was used to compare results before and after treatment of hypertensive cats with amlodipine. The urinary cortisol:cortisone ratio was significantly higher in clinically normal cats (0.87; 0.46-1.39) when compared to NTCKD (0.60; 0.35-1.20; P<0.001), HTCKD (0.62; 0.34-1.00; P=0.002) and cats with iHT (0.65; 0.46-0.85; P=0.015). No statistical difference was detected between NTCKD, HTCKD and iHT groups. No effect of anti-hypertensive treatment on the urinary cortisol-cortisone ratio was detected (P=0.327). Reduced urinary cortisol to cortisone conversion does not appear to be associated with systemic hypertension in cats. In fact, the cortisol to cortisone shuttle appears to be more effective in cats with CKD (hypertensive and normotensive) and iHT than clinically normal cats. The mechanism for this potentially adaptive response to kidney disease is not clear.