Catalase activity and expression are reduced in mesenteric arteries from angiotensin II‐infused hypertensive rats

We have found a NOS‐dependent component of H 2 O 2 production in small mesenteric arteries from hypertensive rats (2.8±0.2 μmol/mg with acetylcholine (ACh) vs. 1.8±0.1 μmol/mg with L‐NAME+ACh; p<0.001; n=9–16), although the mechanism is unknown. The aim of this study was to test the hypothesis that altered antioxidant capability, increased SOD and decreased catalase, contribute to NOS‐mediated H 2 O 2 production in small arteries from hypertensive rats. Normotensive (NORM) and angiotensin II‐infused hypertensive (ANG, 75 ng/min for 2 weeks) rats were studied (n=4–6). Systolic blood pressure increased in ANG compared to NORM (206±2 vs. 110±6 mmHg; p<0.001). Total SOD activity was reduced in homogenates of mesenteric arteries from ANG compared to NORM (3.9±0.4 vs. 6.2±0.8 U/mg; p=0.04). Cu/Zn‐SOD protein expression was reduced in ANG compared to NORM (RDU: 17.0±1.1 vs. 24.5±0.5; p=0.002), whereas Mn‐SOD and ecSOD were not different between groups. Interestingly, both enzymatic activity and protein expression of catalase in ANG were significantly reduced compared to NORM (activity: 7.1±0.7 vs. 10.5±1.6 nmol/min/mg; p=0.05, RDU: 2.4±0.4 vs. 4.6±0.5; p=0.01). In conclusion, we hypothesize that reduced catalase activity and protein expression, not SOD, may contribute to the increased H 2 O 2 level in mesenteric arteries from hypertensive rats.