Neuropathic Pain is caused by damage to a nerve or disease of the somatosensory nervous system. Apart from the blood pressure regulating actions of
angiotensin ligands, studies have shown that it also modulates
neuropathic pain. In the animal models including surgical, chemotherapeutic, and retroviral-induced
neuropathic pain, an increase in the levels of
angiotensin II has been identified and it has been proposed that an increase in
angiotensin II may participate in the induction of
neuropathic pain. The
pain-inducing actions of the
angiotensin system are primarily due to the activation of AT1 and AT2 receptors, which trigger the diverse molecular mechanisms including the induction of
neuroinflammation to initiate and maintain the state of
neuropathic pain. On the other hand, the
pain attenuating action of the
angiotensin system has been attributed to decreasing in the levels of Ang(1-7), and Ang IV and an increase in the levels of
bradykinin. Ang(1-7) may attenuate
neuropathic pain via activation of the spinal Mas receptor. However, the detailed molecular mechanism involved in Ang(1-7) and Ang IV-mediated
pain attenuating actions needs to be explored. The present review discusses the dual role of
angiotensin ligands in
neuropathic pain along with the possible mechanisms involved in inducing or attenuating the state of
neuropathic pain.