Mechanisms of the development of pain in chronic venous diseases, including pelvic congestion syndrome, are not studied in detail so far. The existing hypotheses of the occurrence of venous pelvic pain do not allow to answer the question why some patients have no pain syndrome, while others have very pronounced pain despite the same morphofunctional changes in the pelvic veins. This review presents current hypotheses of the venous pelvic pain development, data on some vasoactive neuropeptides (endothelin, calcitonin gene-related peptide, and substance P), their role in the modulation of vascular tone and sensation of pain, and possible association between neurogenic inflammation and venous pelvic pain, as well as provides rationale for studying the activity of these neurotransmitters in the treatment of pelvic congestion syndrome and pelvic pain.
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