Indirect evidence that purinergic modulation of perivascular adrenergic neurotransmission in the portal vein is a physiological process

Open Access
Publisher Website
Google Scholar
Abstract
The effects of adenine nucleotides and nucleosides on the contractile response to perivascular nerve stimulation were compared in the isolated portal vein of rabbit, rat and guinea‐pig. 2‐Chloroadenosine was more potent than adenosine and ATP, which were equipotent in producing inhibition of neurogenic contractions in the rabbit and rat via prejunctional P1‐purinoceptors. In contrast, neurogenic contractions of the guinea‐pig portal vein were not inhibited by adenosine and were potentiated by 2‐chloroadenosine and, to a lesser extent, by ATP. Fluorescence histochemical localization of quinacrine, which binds to high levels of ATP, revealed a dense perivascular nerve plexus in the portal vein of rabbit and rat but not of guinea‐pig. After chemical sympathectomy, quinacrine‐positive nerves persisted in the rabbit (supporting other evidence for the presence of purinergic nerves) but not in the rat (supporting other evidence for ATP as a cotransmitter in adrenergic nerves). It is concluded that a prejunctional purinergic modulatory mechanism operates in adrenergic neurotransmission in the portal vein of rabbit and rat but not guinea‐pig, and it is suggested that this indicates a physiological mechanism.