To understand the pharmacological mechanism responsible for the stimulatory effects of AJEA on the DCLM contractility, a possible involvement of the muscarinic and/or serotoninergic receptors was investigated using pharmacological strategy.
Regarding in a remarkable difference of contractile patterns produced by AJEA and excitatory neurotransmitters such as ACh and 5-HT (Fig.
Moreover, an obvious stimulatory response to AJEA was observed only in the DCLM, but not in the other regions of GI smooth muscles including the distal colon circular muscles.
Interestingly, AJEA gradually increased the low frequency contraction with high amplitude in the DCLM of rats, and a maximal contraction of DCLM was observed at around 70 min after treating AJEA.
2] receptor-preferring antagonist, methoctramine, abolished only the later phase of contractile response of DCLM to AJEA (Fig.
These cellular events lead us to suppose that activation of serotoninergic receptors also possibly mediates the stimulatory effects of AJEA on the DCLM contractility through enhancing ACh releases.