British journal of pharmacologyAug 2, 2005

Stronger muscle contractions caused by trypsin after estrogen and progesterone treatment in rat uterus

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Updated Apr 3, 2026

Abstract

Both 17beta-estradiol and progesterone enhanced the contractile response to trypsin in a dose-dependent manner, with maximal effects at 25 and 40 mg kg weight(-1) day(-1), respectively.

Pregnant rat myometrium shows enhanced contractility to thrombin and trypsin compared to nonpregnant rats.
Daily injections of 17beta-estradiol or progesterone did not significantly enhance contractions induced by high K(+) or oxytocin.
The enhancement of trypsin-induced contraction in hormone-treated nonpregnant rats was comparable to that seen in pregnant rats.
Thrombin and specific protease-activated receptor (PAR) agonists did not enhance contractile responses in the presence of sex hormones.
PAR1 mRNA levels were low in control myometrium and only slightly increased with progesterone treatment, while PAR2 and PAR4 mRNA were not detected.
A new receptor type, distinct from PAR1, PAR2, or PAR4, may mediate trypsin-induced contractions.

Simplified

We have previously reported that the contractile response to thrombin and trypsin was enhanced in the pregnant rat myometrium. We herein determined whether or not sex hormones contribute to this enhancement and the expression of protease-activated receptors (PARs). The nonpregnant rats received daily injections of either 17beta-estradiol or progesterone, and then the contractile response of the myometrium was examined ex vivo. Treatment with either 17beta-estradiol or progesterone had almost no significant enhancing effect on the high K(+)- or oxytocin-induced contraction. On the other hand, both 17beta-estradiol and progesterone dose-dependently enhanced the contractile response to trypsin. A maximal enhancement was obtained at 25 and 40 mg kg weight(-1) day(-1) for 17beta-estradiol and progesterone, respectively. The extent of the enhancement of the trypsin-induced contraction seen in the sex hormone-treated rats in the present study was comparable to that reported in the pregnant rats. However, the contractile response to thrombin and PAR1/PAR2-AP, SFLLRNP was not enhanced either by progesterone or 17beta-estradiol. PAR2-AP and PAR4-AP failed to induce contraction under any conditions. PAR1 mRNA was scarcely detected in the control myometrium by an RT-PCR analysis, while it slightly increased only in the progesterone-treated rats. Neither PAR2 nor PAR4 mRNA was detected. We thus conclude that the responsiveness to trypsin, but not thrombin, is controlled by sex hormones. A novel type of receptor, other than PAR1, PAR2 or PAR4, is suggested to mediate the trypsin-induced contraction as in the case of the pregnant rat myometrium.

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Stronger muscle contractions caused by trypsin after estrogen and progesterone treatment in rat uterus

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