Abstract
Diabetes is usually associated with alterations in myometrial contractility with altered oxytocin responsiveness that increase the incidence of fetal and maternal morbidity and mortality. Pancreatic β-cells release abscisic acid (ABA) in response to glucose, which in turn potentiates insulin secretion. The aim of the study was to find out the effect of ABA on the uterine contractility in normal and diabetic induced rats and tried to detect its possible underlying signaling pathway. Adult non-pregnant female rats were divided into normal nondiabetic group (n = 27) and diabetic group (n = 12). The effect of ABA on the normal and diabetic isolated myometrium was determined alone or after different blockers. Spontaneous diabetic myometrial contraction showed significant decrease and less responsiveness to oxytocin, KCL, and acetylcholine than nondiabetic samples. ABA showed 60% of oxytocin stimulatory effects on myometrial contraction in a dose-response manner in both groups. Meanwhile, this effect was decreased after blocking L-type calcium channels and completely abolished after blocking prostaglandin F (FP) and inositol trisphosphate (IP3) receptors. ABA is found to have an uterotonic effect that is mediated mainly via FP receptor through increasing the level of IP3. So, ABA by its novel effect could be beneficial as pre-labor prescription, especially in diabetic females.
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