EFFECTS OF EXPERIMENTALLY INDUCED DIABETES MELLITUS ON PHARMACOLOGICALLY AND ELECTRICALLY ELICITED MYOMETRIAL CONTRACTILITY

Mar 21, 2009Clinical and experimental pharmacology & physiology

How induced diabetes affects drug- and electrical-stimulated uterine muscle contractions

AI simplified

Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

Approximately 7% of pregnancies are affected by diabetes, which may alter uterine contractility.

Electrical stimulation of uterine rings from diabetic rats showed continuously low sensitivity compared to intact rats.
Diabetes increased noradrenaline-induced contractions and decreased relaxation to terbutaline in non-pregnant rats.
Diabetic non-pregnant rats exhibited higher levels of α1B-adrenoceptors and lower levels of α1D-adrenoceptors.
In late pregnancy, oxytocin enhanced contractility in diabetic rats without changing its effective concentration.
Higher expression of oxytocin receptors was found in the myometrium of diabetic rats during late pregnancy.
Experimental diabetes may increase sensitivity to oxytocin and influence uterine contractions in diabetic pregnancies.

AI simplified

1. Diabetes is one of the most frequent complications of gestation, affecting approximately 7% of pregnancies. However, little is known about its effects on electrically and pharmacologically stimulated myometrial contractility. The aim of the present study was to investigate the consequences of streptozotocin (STZ)-induced diabetes on: (i) electrical field stimulation (EFS)-evoked contraction of isolated uterine rings as a function of gestational age; and (ii) the uterotonic and tocolytic actions of α- and β-adrenoceptor stimulation, respectively. The effects of oxytocin in late pregnancy were also investigated. 2. During pregnancy, EFS-evoked contractions of isolated uterine rings from intact rats declined, whereas isolated uterine rings from diabetic rats exhibited continuously low sensitivity to EFS. 3. In non-pregnant rats, diabetes resulted in increased noradrenaline-mediated contractility and a decreased relaxation response to terbutaline. At the mRNA level, diabetes enhanced the expression of α1B-adrenoceptors in non-pregnant rats from 14.65 to 18.39 μg/mL (P < 0.05), whereas the expression of α1D-adrenoceptors decreased (from 42.87 to 35.67 μg/mL; P < 0.05). During pregnancy, the responses to these sympathomimetics did not differ between diabetic and intact rats. 4. In late pregnancy (on Days 15 and 21), oxytocin caused greater maximum contractility of uterine rings from diabetic rats without affecting the EC(50). In addition, on Day 15 of pregnancy, the expression of oxytocin receptors in the myometrium of diabetic rats was higher than that in intact rats. 5. The results of the present study indicate that experimental diabetes facilitates gestation-induced denervation and increases myometrial sensitivity to oxytocin in late pregnancy. If similar mechanisms operate in humans, this could contribute to a tendency to premature uterine contractions in diabetes-complicated pregnancies.

Full Text

Full text is available at the source.

View full text ↗

EFFECTS OF EXPERIMENTALLY INDUCED DIABETES MELLITUS ON PHARMACOLOGICALLY AND ELECTRICALLY ELICITED MYOMETRIAL CONTRACTILITY

Abstract

Full Text

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the circadian biology brief

Abstract

Full Text

Related papers

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the circadian biology brief