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Role of endothelium in the human uterine arteries during normal menstrual cycle
Author(s) -
Azuma Hiroshi,
Obayashi Satoshi,
Hamasaki Hidehisa,
Koyama Takao,
Aso Takeshi
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb13289.x
Subject(s) - sodium nitroprusside , endocrinology , contraction (grammar) , luteal phase , acetylcholine , medicine , chemistry , endothelium , follicular phase , menstrual cycle , methylene blue , vasodilation , nitric oxide , hormone , biochemistry , photocatalysis , catalysis
1 The present experiments were designed to investigate the role of endothelium in the human uterine arteries during the normal menstrual cycle. 2 Acetylcholine (ACh) produced a concentration‐dependent relaxation response during the higher level of plasma 17β‐oestradiol (E 2 ) (follicular and luteal phases, E 2 = 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 (E 2 = 19.8 ± 2.9 pg mg −1 , n = 5; group II). During the follicular and luteal phases (E 2 = 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 ( P <0.05 and P <0.005) reduced in group III. Sodium nitroprusside (SNP)‐induced relaxation was similar in the three groups. 3 Correlation between the maximum response to ACh and the plasma E 2 was highly significant (γ = 0.8142, P <0.001) in 18 cases of groups I and II, but not in all 24 cases including group III (γ = 0.1183, NS). 4 Relaxations in response to ACh in group I or A23187 in all groups were abolished after removal of the endothelium. In group I, ACh‐ and A23187–induced relaxations were greatly inhibited by methylene blue or N 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. 5 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. 6 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. 7 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 (PGI 2 ) 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 PGI 2 might play a role in the formation of intimal thickening in human uterine arteries.