Hindlimb skeletal muscle stretch (i.e., selective activation of the muscle mechanoreflex) in decerebrate rats evokes reflex increases in blood pressure and sympathetic nerve activity. Bradykinin has been found to sensitize mechano-gated channels through a bradykinin B2 receptor-dependent mechanism. Moreover, bradykinin B2 receptor expression on sensory neurons is increased following chronic femoral artery ligation in the rat (a model of simulated peripheral artery disease). We tested the hypothesis that, in decerebrate, unanesthetized rats, the injection of bradykinin into the arterial supply of a hindlimb would acutely augment (i.e., sensitize) the increase in blood pressure and renal sympathetic nerve activity (RSNA) during hindlimb muscle stretch to a greater extent in rats with a ligated femoral artery than in rats with freely perfused femoral arteries. The pressor response during static hindlimb muscle stretch was compared before and after the hindlimb arterial injection of 0.5 µg of bradykinin. The injection of bradykinin itself increased blood pressure to a greater extent in "ligated" rats (n=10) than in "freely perfused" rats (n=10). The increase in blood pressure during hindlimb muscle stretch, however, was not different before compared to after bradykinin injection in either freely perfused (control: 14±2, post-bradykinin: 15±2 mmHg, p=0.62) or ligated (control: 15±3, post-bradykinin: 14±2 mmHg, p=0.80) rats. Likewise, the increase in RSNA during stretch was not different before compared to after bradykinin injection in either group of rats. We conclude that bradykinin does not acutely sensitize the pressor response during hindlimb skeletal muscle stretch in either freely perfused or ligated decerebrate rats.