Sex differences in CGRP-induced vasodilation of human middle meningeal arteries but not human coronary arteries: implications for migraine

Author:

de Vries Tessa1ORCID,Boucherie Deirdre M.1,Chan Kayi Y.1,Rubio-Beltrán Eloísa1,Labastida-Ramírez Alejandro1,Labruijere Sieneke1,Gupta Saurabh1,van den Bogaerdt Antoon2,Vincent Arnaud3,Dammers Ruben3,Danser A. H. Jan1,MaassenVanDenBrink Antoinette1

Affiliation:

1. Division of Vascular Medicine and Pharmacology, Department of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, The Netherlands

2. Heart Valve Department, ETB-BISLIFE, Beverwijk, The Netherlands

3. Department of Neurosurgery, Erasmus MC, University Medical Center Rotterdam, The Netherlands

Abstract

Background Migraine prevalence and levels of calcitonin gene-related peptide (CGRP), a peptide involved in migraine pathophysiology, differ between men and women, and appear to be affected by changes in sex hormones. The present study investigated the sex-specific responses to CGRP in human isolated arteries. Methods CGRP-induced relaxation of 62 (28 men and 34 women) human isolated middle meningeal arteries (HMMA) and 139 (69 men and 70 women) human isolated coronary arteries (HCA) was compared between men and women in groups <50 years and ≥50 years of age as a proxy for pre- and postmenopausal status in women, as well as matched-age groups for men. Results In HCA, no differences were observed between male and female tissue, or between the different age groups. However, in HMMA, the maximum response was significantly smaller and CGRP was less potent in females <50 compared with males <50 years of age. No differences were observed between the older age groups. Conclusions Sex differences were observed for CGRP-induced relaxation of HMMA, but not HCA. These differences could arise from differential receptor expression in the vascular beds combined with the effect of sex hormones on CGRP and subsequent receptor desensitization.

Funder

Nederlandse Organisatie voor Wetenschappelijk Onderzoek

Publisher

SAGE Publications

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