Role of endogenous carbon monoxide in hypertension pathogenesis of rats

The present study investigated the contribution of endogenous heme oxygenase (HO)/carbon monoxide (CO) system to hypertension pathogenesis of rats. Zinc deuteroporphyrin 2,4-bisglycol (ZnDPBG), an inhibitor of heme oxygenase (HO), was used to inhibit HO activity in vivo. It was found that the blood pressure of rats with HO inhibition was significantly elevated, and plasma levels of adrenaline, noradrenaline, endothelin, nitrate and nitrite were significantly increased. HO activity and HbCO formation within vascular smooth muscle tissues were significantly inhibited after administration of ZnDPBG. Furthermore, administration of exogenous CO into HO inhibiting rats led to MABP decrease, but injection of HO substrate, heme-L-lysinate, had no effect on HO inhibition-induced hypertension. In spontaneously hypertensive rats, injection of exogenous CO resulted in a significant decrease of MABP, and heme-L-lysinate had a similar effect with exogenous CO. These data show that HO/CO system has an anti-hypertension biological action, suggesting that endogenous CO plays an important role in hypertension pathogenesis.