The Differences of Pain Receptor and Pain-Related Neurotransmitters in the Vagina of Pre- and Post- Menopausal Women

2021 ◽  
Vol 104 (3) ◽  
pp. 375-382
Keyword(s):  
Substance P ◽  
Stromal Cells ◽  
Related Protein ◽  
Cgrp Receptor ◽  
Calcitonin Gene ◽  
Menopausal Women ◽  
Protein Expressions ◽  
Vaginal Pain ◽  
Substance P Receptor ◽  
Post Menopausal

Objective: Post-menopausal vaginal pain and burning sensation are not solely relieved by improving vaginal dryness. Stimulation of pain receptor (nociceptor) may be a part of the post-menopausal vaginal pain mechanism. The authors primarily evaluated the level of substance P receptor in pre- and post-menopausal women and secondarily studied the level of calcitonin gene-related peptide (CGRP) receptor and nociceptor-activating substances in pre- and post-menopausal women. The association between vaginal pain score and the change in nociceptor and nociceptoractivating substances was analyzed. Materials and Methods: A cross-sectional study was conducted in 122 pre- and post-menopausal women that underwent total abdominal hysterectomy. Vaginal specimens were obtained and stained for substance P receptor, substance P, CGRP receptor and CGRP, which were used as nociceptive parameters in the present study. Vaginal stromal cells were counted for pain-related protein expressions. Mean pain-related protein expressions in vaginal stromal cells were compared between pre- and post-menopausal women. Results: Fifty-eight pre-menopausal women and 33 post-menopausal women were included for analysis. Mean substance P receptor, substance P, CGRP receptor and CGRP in post-menopausal women were higher than in pre-menopausal women (47.69, 42.32, 71.31 and 60.73 cells, respectively for post-menopausal women, and 22.03, 21.54, 41.45 and 35.80 cells, respectively for pre-menopausal women). These differences were under the major influence of hormonal status rather than age. The changes in mean pain-related protein expression in vaginal stromal cell after menopause were highest in the first two years. No difference in mean pain-related protein expression in vaginal stromal cell was observed between pain and no pain groups. Conclusion: In the present study, post-menopausal women were found to have higher mean pain-related protein expressions in vaginal stromal cells than pre-menopausal women. Keywords: Post-menopausal women, Vaginal pain, Vaginal dryness, Vaginal burning sensation, Vaginal nerve, Substance P, CGRP, Calcitonin gene-related peptide

Mechanisms of glyceryl trinitrate provoked mast cell degranulation

Cephalalgia ◽  
2015 ◽  
Vol 35 (14) ◽  
pp. 1287-1297 ◽  
Author(s):  
Sara Hougaard Pedersen ◽  
Roshni Ramachandran ◽  
Dipak Vasantrao Amrutkar ◽  
Steffen Petersen ◽  
Jes Olesen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mast Cell ◽  
Substance P ◽  
Glyceryl Trinitrate ◽  
Receptor Antagonist ◽  
Ex Vivo ◽  
Mast Cell Degranulation ◽  
Nitric Oxide Donor ◽  
Calcitonin Gene ◽  
Substance P Receptor

Background Migraine patients develop attacks several hours after intravenous infusion of glyceryl trinitrate. Due to the short half-life of nitric oxide, this delayed migraine cannot be caused by a direct action of nitric oxide derived from glyceryl trinitrate. The involvement of meningeal inflammation and dural mast cell degranulation is supported by the effectiveness of prednisolone on glyceryl trinitrate-induced delayed headache. Methods Using a newly developed rat model mimicking the human glyceryl trinitrate headache model, we have investigated the occurrence of dural mast cell degranulation after a clinically relevant dose of glyceryl trinitrate. Results A 6-fold increase in degranulation was observed starting at 2 hours after glyceryl trinitrate infusion. Interestingly, pre-treatment with the effective anti-migraine substances L-nitro-arginine methyl ester and sumatriptan prevented glyceryl trinitrate-induced mast cell degranulation whereas the calcitonin gene-related peptide-receptor antagonist olcegepant and the substance P receptor antagonist L-733,060 did not affect mast cell degranulation. However, topical application of two different nitric oxide donors did not cause mast cell degranulation ex vivo. Conclusions Direct application of an exogenous nitric oxide donor on dural mast cells does not cause mast cell degranulation ex vivo. In vivo application of the nitric oxide donor glyceryl trinitrate leads to a prominent level of degranulation via a yet unknown mechanism. This effect can be completely blocked by inhibition of the endogenous nitric oxide production and by 5-HT1B/1D receptor agonists but is unaffected by calcitonin gene-related peptide and substance P receptor antagonists.

The Effects of Therapy with Oestriol Succinate and Ethinyl Oestradiol on the Haemostatic Mechanism in Post-Menopausal Women

1976 ◽  
Vol 35 (02) ◽  
pp. 403-414 ◽  
Author(s):  
Terence Davies ◽  
Gillian Fieldhouse ◽  
George P. McNicol
Keyword(s):  
Coagulation Factors ◽  
Factor Vii ◽  
Oestrogen Therapy ◽  
Qualitative And Quantitative ◽  
Lysis Activity ◽  
Menopausal Women ◽  
Increased Sensitivity ◽  
Post Menopausal ◽  
Incremental Increase ◽  
Ethinyl Oestradiol

SummaryThe effects on the haemostatic mechanism of oestrogen therapy, given to prevent bone loss in post-menopausal women, have been investigated. Oestriol succinate was given orally to 10 women at a level of 2 mg/day for 1 month and for a further 3 months with incremental increase of 2 mg each month. 6 of the 10 women were subsequently treated with 25 μg/day orally of ethinyl oestradiol. Oestriol succinate therapy resulted in a small increase in the level of factor VII, a decrease in factor VIII concentration and increased sensitivity of platelets to aggregating agents. Ethinyl oestradiol treatment resulted in much more widespread changes with marked increases in coagulation factors VII, VIII, IX and X, decreased levels of antithrombin and dramatic increases in circulating plasminogen levels and euglobulin lysis activity. The data suggested that the nature of oestrogens employed therapeutically is important in determining the qualitative and quantitative effect of oestrogen therapy on components of the haemostatic mechanism.

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