Adrenoceptor modulated flow through the XXXX ampulloisthmic region studied in vivo and in vitro.

@entity1 @entity1169 @entity3465 @entity95 @entity5333 @entity2647 @entity815 @entity1063 @entity4183
In adult @entity95 does ovulation was induced by @entity1 choriongonadotropin (hCG) 48 hours before experiments. At laparotomy the oviducts were cannulated from the ovarian and uterine ends. In vivo as well as in vitro the patency of the isthmus was studied with low viscous fluid perfusion of the ampulloisthmic region in antegrade direction. Intraluminally applied @entity1063 (NE) or @entity2647 ( @entity815 ) caused dual changes in transisthmic flow; administration of a low dose increased the flow, while high doses decreased the flow in vivo. In vitro, application of PhE only induced a dose-dependent reduction of flow. The PhE-induced reduction of flow was prevented by pretreatment with @entity5333 in vivo and in vitro, suggesting activation of an alpha-adrenoceptor mechanism. Intraluminal application of @entity4183 (T) caused a dose-dependent increase of flow, which was most prominent in vivo. Such an increase of flow was prevented by blockade of beta-adrenoceptors with @entity1169 or by selective blockade of beta 2-adrenoceptors with @entity3465 399 both in vivo and in vitro, indicating activation of a beta 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 ampulloisthmic 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 of alpha-adrenoceptors in support of such a hypothesis. However, it must be noted that this region also possesses a population of beta-adrenoceptors at this time interval, which may interfere with a constrictor mechanism via circulating epinephrine.
