Arginase in the airways hyperreactivity

The interest of arginase action is increasing because limitation of L-arginine bioavailability by arginase for NO synthesis via constitutive NOS can contribute to airway hyperreactivity.

We investigated the effect of intervention in the arginase activity in guinea pig model of experimental ovalbumin-induced airway hyperreactivity.

We analysed the response of tracheal and lung tissue smooth muscle strips to histamine or acetylcholine after in vitro administration of arginase in a dose of 75 UI or after administration of the non-selective inhibitor of arginase N(omega)-hydroxy-L-arginine (NOHA) in a dose of 5 and 10 micromol. We used as well as the incubation of strips with the precursor of NO synthesis L-arginine in a dose of 10(-4) mol/l together with NOHA.

We did not find any significant differences in the reactivity of tracheal and lung tissue smooth muscle if we applied arginase in a dose of 75 UI in vitro. NOHA in a dose of 5 a 10 micromol induced the decrease of tracheal and lung tissue smooth muscle reactivity overall. The decrease of the contraction amplitude was dose-dependent. The supplementation of NO synthesis precursor L-arginine in a dose of 10(-4) mol/l together with NOHA intensified the decrease of the airways reactivity induced by an arginase inhibition.

The results suggest that arginase is involved in the control of airways bronchomotoric tone and therefore modulation of arginase activity could be a useful tool for airway smooth muscle tone control in clinical conditions (Fig. 7, Ref. 33). Full Text (Free, PDF) www.bmj.sk.