It is possible that besides NO as manifested by an increase in eNOS expression and anti-inflammatory activity of CO as documented by the fall in COX-2 and iNOS expression in rats with and without sensory denervation, the TRPV1/CGRP-α system can be involved in gastric hyperemia associated with this protection induced by CO released from its donor, CORM-2. Here, TRPV1 is linked to hyperemia.