How Could Aortic Arginase Activity Enhancement Be Involved in DOCA‐Salt Hypertension?

Abstract

This study was to examine whether the increase in aortic arginase activity observed in DOCA‐salt hypertensive rats is involved in the mechanism of physiological hypertension by participating to vessel hypertrophy and/or to the impairment of endothelium‐dependent relaxation to acethylcholine. We measured polyamine content and relaxation‐response to acethylcholine in aortic rings isolated from control and DOCA‐salt treated Sprague–Dawley rats after in vitro modification of arginase activity. Polyamine content was significantly increased in aorta from DOCA‐salt hypertensive rats compared with controls. In the normotensive rats, the addition of L‐valine (an inhibitor of arginase) decreased the relaxation response to acethylcholine whereas the addition of arginase increased the relaxation dependent response. On the contrary, in DOCA‐salt hypertensive rats, the addition of L‐valine or of arginase did not change the endothelium dependent relaxation. The results obtained suggest that the increase in aortic arginase activity in DOCA‐salt hypertension could contribute to vascular hypertrophy but not to the impairment of endothelium‐dependent relaxation.

• DOCA‐salt hypertension
• Aorta
• Arginase
• Polyamine
• Endothelium‐dependent relaxation
• NO