A study of the mechanisms involved in relaxation induced by 17-beta-estradiol in the isolated rabbit aorta.
We used the isolated rabbit aorta to examine the mechanisms that mediate the known vasodilatation induced by 17-beta-estradiol. Our results suggest that nitric oxide (NO), the inhibition of Ca2+ release from intracellular stores through the IP3 pathway and Ca2+ influx through potential-dependent calcium channels (PDCs) seem to be involved. Prostaglandins and adrenergic beta receptors do not influx, intracellular Ca2+ release, NO, cyclic guanine monophosphate (cGMP), prostaglandins and adrenergic beta receptors.
Li
H-F
HF
Department of Physiology, Lanzhou Medical College, Gansu Province, People's Republic of China. LHOF@163.net
Li
W
W
Zheng
T Z
TZ
Qu
S Y
SY
Zhang
C L
CL
D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004594:Electrophysiology; D004730:Endothelium, Vascular / Q000502:physiology; D004958:Estradiol / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D009569:Nitric Oxide / Q000502:physiology; D011188:Potassium / Q000494:pharmacology; D011817:Rabbits; D014664:Vasodilation / Q000502:physiology
D015220:Calcium Channels; D009569:Nitric Oxide; D004958:Estradiol; D011188:Potassium; D002118:Calcium