Oral contraceptive administration attenuates endothelium-dependent relaxation in response to histamine but not to acetylcholine in aortic rings of female rats.
The incidence of vascular disorders is markedly lower in cycling, pre-menopausal women and post-menopausal women receiving estrogen-progestogen therapy than in men or untreated postmenopausal women. Clinical studies demonstrate that estrogen-progestogen therapy in pre-menopausal women is associated with increased arterial vascular risk. However, the mechanism of estrogen-progestogen therapy in arterial vascular complications remain unclear. Therefore, the present study aimed at investigating whether chronic administration of combined oral contraceptive (OC) containing progestogen with androgenic property alters endothelium-dependent relaxation responses of the aorta to histamine and acetylcholine. The experiments have been studied on aortic rings obtained from vehicle-treated and OC-treated female Sprague-Dawley rats. Isometric reactivity of aortic rings was recorded with a strain gauge transducer. The maximum contractile response of the aortic rings to noradrenaline in the OC-treated group was not significantly different from that in the vehicle-treated group. Both acetylcholine and histamine caused relaxation of the noradrenaline pre-contracted aortic rings. The relaxation response to acetylcholine in rings from vehicle-treated and OC-treated rats did not differ significantly, while relaxation response to histamine was significantly attenuated in aortic rings from OC-treated rats. In conclusion, the results from the present study suggest that the increased arterial vascular risk associated with OC administration might involve altered endothelium-dependent relaxation via histaminergic-mediated mechanism, but not via muscarinergic-mediated mechanism.
Olatunji
Lawrence Aderemi
LA
Department of Physiology, College of Health Sciences, University of Ilorin, Ilorin, Nigeria. tunjilaw04@yahoo.com
Soladoye
Ayodele Olufemi
AO
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000502:physiology; D018376:Cardiovascular Abnormalities / Q000453:epidemiology / Q000503:physiopathology; D003276:Contraceptives, Oral / Q000494:pharmacology*; D004347:Drug Interactions; D004730:Endothelium, Vascular / Q000187:drug effects*; D005260:Female; D006632:Histamine / Q000494:pharmacology*; D017442:Histamine Agonists / Q000494:pharmacology; D015994:Incidence; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology
D003276:Contraceptives, Oral; D017442:Histamine Agonists; D014665:Vasodilator Agents; D006632:Histamine; D000109:Acetylcholine