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Beta-estradiol induced catecholamine-sensitive hyperalgesia: a contribution to pain in Raynaud's phenomenon.

The physiological basis of the pain and hyperalgesia observed in patients with Raynaud's phenomenon (RP) is unknown. Since estrogen-induced effects on sympathetic postganglionic neurons (SPGNs) have been implicated in the vasomotor abnormalities in patients with RP, we have studied the effects of estradiol on nociceptive thresholds and noradrenaline sensitivity in a nociceptive flexion reflex in the rat. We report that estradiol induces a catecholamine sensitive hyperalgesia. This hyperalgesia is antagonized by yohimbine (an alpha 2-adrenergic antagonist) but not prazosin (an alpha 1-adrenergic antagonist) as well as by inhibitors of the cyclooxygenase pathway of arachidonic acid metabolism. These data are compatible with the hypothesis that the sensory abnormalities observed in patients with RP may depend on estradiol-induced changes in SPGN, resulting in a sympathetically-dependent production of cyclooxygenase products of arachidonic acid.