Abstract
We aimed to prospectively examine β-adrenoceptor-mediated uterine contractility in women suffering from gynecological malignancies. Myometrial specimens were obtained from non-pregnant women undergoing hysterectomy for benign gynecological disorders, and ovarian, endometrial, synchronous ovarian–endometrial, and cervical cancer. Contractions of myometrial strips in an organ bath before and after cumulative dosages of β2- and β3-adrenoceptor agonists with preincubation of propranolol, SR 59230A, and butoxamine were studied. All agonists induced a dose-dependent attenuation for uterine contractility in endometrial or cervical cancer, similar to that observed in the reference group. Contradictory effects were observed for ovarian cancer alone or in combination with endometrial cancer. CL 316243 or ritodrine abolished the relaxation, whereas BRL 37344 increased the uterine contractility in ovarian cancer. Moreover, β-adrenoceptor antagonists caused varied effects for β2- or β3-adrenoceptor agonists. Our experiments demonstrate that ovarian cancer, alone or as synchronous ovarian–endometrial cancer, substantially alters uterine contractility in response to β-adrenoceptor agonists.
Highlights
Electronic supplementary material The online version of this article contains supplementary material, which is available to authorized users.There is a growing body of evidence that adrenergic signaling, a central mediator of stress, affects numerous cellular processes that are critical for carcinogenesis [1,2,3]
All agonists induced a dose-dependent attenuation for uterine contractility in endometrial or cervical cancer, similar to that observed in the reference group
Our experiments demonstrate that ovarian cancer, alone or as synchronous ovarian–endometrial cancer, substantially alters uterine contractility in response to badrenoceptor agonists
Summary
There is a growing body of evidence that adrenergic signaling, a central mediator of stress, affects numerous cellular processes that are critical for carcinogenesis [1,2,3]. Adrenergic signaling can affect an extensive range of cancer-related molecular pathways via regulation of b-adrenoceptor-bearing tumor cells and other cells present in the tumor’s microenvironment [2, 4]. B2-Adrenoreceptor agonists, such as ritodrine or salbutamol, are the most commonly used tocolytic agents. Their benefits are limited because of associated significant adverse cardiovascular effects [12, 13]. There is in vitro evidence that the potential cardiovascular effects of b3-adrenoreceptor agonists is less than that of b2-adrenoreceptor agonists [14]. Before b3-adrenoreceptor agonists become therapeutic drugs with a potential target for
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
