The modern notion of pain and its clinical management, along with its physiological origins, is of exceeding interest to both clinicians and basic science researchers. While much is known about the control of pain via non-steroidal anti-inflammatory medications or comparative exogenous analgesics, little is known about the interplay between pain perception and its relationship with catecholamine molecules. We believe that the perception of pain and the body's self-attempt to alleviate it utilizing conventional homeostatic mechanisms via endogenous opiate release is mediated by key catecholamines, and that this effect is further modulated by nitric oxide. We further propose a new paradigm which links pain, endogenous opiates, and the catecholamines in a unique robust fashion demonstrating a complex symbiotic signaling system.

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