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All efforts to develop nonsteroidal anti-inflammatory drugs (NSAIDs) which are devoid of gastrointestinal and cardiovascular system effects are still far from achieving a breakthrough.In contrast, no effect was observed for the COX-inhibitor diclofenac in both stress- and corticosterone-induced hyperalgesia.The results indicate that a dysregulated corticosterone secretion leads in both hyperalgesia models to glucocorticoid receptor alterations, resulting in an increased pain perception due the influence on nociception-modulating neurotransmitters.The lymphocytes of these animals showed a reduced sensitivity of glucocorticoid receptors with an accompanied increase of receptor density, which is assumed to be an attempted decompensation mechanism.Furthermore, it supposed that the observed glucocorticoid receptor alterations may contribute to increased pain sensitivity, since a number of nociception-modulating neurotransmitters is affected by this receptor.

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