Adrenoceptor modulated flow through the rabbit ampulloisthmic region studiedin vivo andin vitro

Abstract

In adult rabbit does ovulation was induced by human choriongonadotropin (hCG) 48 hours before experiments. At laparotomy the oviducts were cannulated from the ovarian and uterine ends.In vivo as well asin vitro the patency of the isthmus was studied with low viscous fluid perfusion of the ampulloisthmic region in antegrade direction. Intraluminally applied nor-epinephrine (NE) or phenylephrine (PhE) caused dual changes in transisthmic flow; administration of a low dose increased the flow, while high doses decreased the flowin vivo. In vitro, application of PhE only induced a dosedependent reduction of flow. The PhE-induced reduction of flow was prevented by pretreatment with phenoxybenzaminein vivo andin vitro, suggesting activation of anα-adrenoceptor mechanism. Intraluminal application of terbutaline (T) caused a dosedependent increase of flow, which was most prominentin vivo. Such an increase of flow was prevented by blockade ofβ-adrenoceptors with propranolol or by selective blockade ofβ ₂-adrenoceptors with IPS 399 bothin vivo andin vitro, indicating activation of aβ ₂-adrenoceptor mechanism. The biochemical and hormonal changes 48 hours after ovulation imply a role for the sympathetic transmitter NE in causing a contractile state of the ampullo-isthmic region (“tube locking”) for retention of ova prior to nidation in the uterine cavity. The isthmus would then hypothetically act as a sympathetically innervated smooth muscle sphincter. The present results demonstrate a constrictory response of this region to high-dose stimulation ofα-adrenoceptors in support of such a hypothesis. However, it must be noted that this region also possesses a population ofβ-adrenoceptors at this time interval, which may interfere with a constrictor mechanism via circulating epinephrine.