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The role of renal angiotensin converting enzyme (ACE) in blood pressure regulation is not well understood. In our studies, both acute and chronic treatment of hypertensive rats SHR and SHRSP with ACE inhibitors Enalapril and SA446 had a blood pressure lowering effect that coincided with an inhibition of renal cortical and aortic ACE, but not plasma ACE. Further, ACE activities in the renal cortex and aorta were found to increase with aging of the SHRSP, therefore concomitantly with hypertension development. In the kidney, brush border membranes (BBM) contained abundant ACE. We found that the activities of ACE in the renal cortex closely correlated to the activities in isolated BBM, in Wistar Kyoto rats and in the SHRSP. Thus, renal cortical ACE activity and blood pressure correlated in cases of ACE inhibition and hypertension development. Since the ACE activity in the renal cortex appeared to reflect the enzyme activity in BBM, the brush border ACE may have to be taken into account, in view of the relationship between renal ACE and blood pressure.

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The activities of angiotensin converting enzyme (ACE) in crude extracts of renal cortex, heart and brain of the rat were increased when the oxidizing agent diamide was added to the extracts and then the activity determined. By pretreatment of the extracts with 10 mM diamide, the activities of ACE in the extracts of heart, brain and renal cortex were about 500, 290 and 240% of the control value, determined without the diamide-pretreatment, respectively. In the lung and aorta, increments in the activity after oxidation were less than 20% of the control. No such increase was observed in the plasma. Similar results were obtained when the extracts were exposed to O2. The activity was also increased by oxidation with diamide and O2, when an extract of the human renal cortex was used. Thus, the activity of ACE in the kidney, heart and brain can be increased by oxidation.