Role of endothelium in the human uterine arteries during normal menstrual cycle

Open Access
Publisher Website
Google Scholar
Abstract
The present experiments were designed to investigate the role of endothelium in the human uterine arteries during the normal menstrual cycle. Acetylcholine (ACh) produced a concentration‐dependent relaxation response during the higher level of plasma 17β‐oestradiol (E2) (follicular and luteal phases, E2 = 131.9 ± 15.9 pg ml−1, n = 13; group I). However, the agent did not produce a definite relaxation, but produced a slight contraction during the ovulatory and menstruation phases (E2 = 19.8 ± 2.9 pg mg−1, n = 5; group II). During the follicular and luteal phases (E2 = 181.1 ± 9.0 pg ml−1, n = 6), ACh produced a slight contraction, but not relaxation in 6 cases (group III). Relaxation in response to A23187 in group II was not different from that in group I, while it was significantly (PP 2 was highly significant (γ = 0.8142, P G‐nitro‐l‐arginine (l‐NOARG) and partially inhibited by indomethacin. None of these treatments except for methylene blue modified the SNP‐induced relaxation, which was significantly inhibited by methylene blue. The A23187‐induced relaxation was hardly affected by methylene blue or l‐NOARG in group III, but was partially inhibited by these agents in group II. The effect of indomethacin in inhibiting the A23187 induced‐relaxation was most potent (58.9%) in group III and least (16.9%) in group I. There were no histological changes in 14 cases out of 18 (groups I and II), but very slight intimal thickening was observed in 4 cases in group I. On the other hand, severe intimal thickening was observed in all 6 cases in group III. These results indicate that, in human uterine artery strips, ACh and A23187 cause endothelium‐dependent relaxations, which are mediated mainly through EDRF/NO in group I, mainly prostacyclin (PGI2) in group III, or both in group II. It is suggested that lack of the production/release of EDRF/NO and/or of interaction between EDRF/NO and PGI2 might play a role in the formation of intimal thickening in human uterine arteries.