In vitro effects of endothelin-1 on the contractility of myometrium obtained from pre- and postmenopausal women

Ekaterini Domali, E. Asprodini, P. A. Molyvdas, Ioannis E. Messinis
In: Journal of Endocrinology · 2001 · vol. 168(1) , pp. 153–162 · doi:10.1677/joe.0.1680153 · PMID:11139779 · W2104059211
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⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

Endothelin-1 increased myometrial contractility and basal tone, with postmenopausal myometrium showing a stronger, sustained contraction than premenopausal myometrium.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

This in vitro study examined how endothelin-1 (ET1) affects contractility of human nonpregnant myometrium obtained from hysterectomy patients in premenopausal follicular (n=14), premenopausal luteal (n=20), and postmenopausal (n=12) hormonal states, using isometric recording of uterine strips exposed to ET1 (10^-16 to 10^-10 M) and, in comparison, KCl (80 mM) alone or with ET1. ET1 at 10^-16 M induced weak, ripple-like contractions with longer duration and higher contractile measures in luteal vs follicular tissue, whereas in postmenopausal tissue ET1 produced sustained contractions with obliteration of spontaneous contractility and marked increases in amplitude and area under the contractility curve. Combining ET1 with KCl reproduced ET1-like contractility patterns but prolonged effects compared with KCl alone, and basal-tone changes differed between KCl and ET1 in postmenopausal tissue, supporting distinct mechanisms. A key limitation is that tissue viability and responsiveness were assessed mainly by immediate KCl responsiveness within a short post-hysterectomy window, and hormone groups were defined by measured peripheral estradiol/progesterone rather than detailed tissue-level receptor/ET pathway analysis. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

This study was conducted to evaluate the responsiveness of human nonpregnant myometrium to endothelin 1 (ET1) (10(-10) M-10(-6 )M) and KCl (80 mM) in relation to the hormonal profile of the women, who were allocated into three groups: group 1, premenopausal follicular phase, n=14, group 2, premenopausal luteal phase, n=20, and group 3, postmenopausal women, n=12. At a concentration of 10(-6 )M, ET1 in both groups 1 and 2 induced very low ripples of high frequency (group 1: 80+/-14%, n=5, group 2: 314+/-63%, n=11; P<0.05 compared with the pretreatment frequency) which lasted significantly longer in group 2 (29+/-2 min, n=10, P<0.05) than in group 1 (20+/-2 min, n=5), increasing the basal tone (group 1: 57.9+/-6%, n=5, group 2: 64.4+/-4%, n=6), the amplitude of myometrial contractility (group 1: 1.2+/-0.07 g, n=5, group 2: 1.6+/-0.1 g, n=7, P<0.05) and the area under the contractility curve (AUC; group 1: 8.4+/-1.1 gxmin, n=6, group 2: 11.9+/-1.6 g x min, n=11). In group 3, ET1 (10(-6 )M) created a sustained long-lasting contraction (initial phase: 43+/-6 min, n=6) characterized by the complete obliteration of spontaneous contractility with no ripples at all, and increasing significantly (P<0.05) the amplitude of myometrial contractility (2.8+/-0.5 g, n=6), the AUC (24.7+/-3.3 g x min, n=6), as well as the basal tone (183.6+/-21%, n=6) compared with the two premenopausal groups. In all three groups KCl exposure induced an initial rise (mean amplitude value: 1.1 g) followed by a relaxation phase to the primal baseline level (mean duration value: 12 min). Addition of ET1 (10(-6 )M) to KCl (80 mM) induced a similar pattern of contractility to that evoked by ET1 alone which, compared with KCl alone lasted significantly longer (P<0.05) in all three groups (group 1: 20+/-2 min, n=6; group 2: 23+/-2 min, n=6; group 3: 35+/-3 min, n=5). In group 3, the percentage change in basal tone was significantly smaller following KCl than after the combination of KCl plus ET1 (149+/-16%, n=5; P<0.01), indicating a different mechanism of contractility between KCl and ET1. These results demonstrate for the first time differences in myometrial response to ET1 between pre- and postmenopausal women. It is suggested that KCl and ET1 affect uterine contractility through different mechanisms and that ovarian steroids may play a regulatory role in human uterine responsiveness to ET1.

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