Effects of reserpine on nerve stimulation-induced constrictions in canine isolated splenic artery

1. Our previous studies have demonstrated that peri-arterial electrical nerve stimulation (PNS) of the canine splenic artery induces a double-peaked vasoconstriction consisting of an initial transient, dominantly P2X purinoceptor-mediated constriction, followed by a prolonged, mainly alpha1-adrenoceptor-induced response. In the present study, we examined the effects of reserpine on PNS-induced double-peaked responses. 2. The vasoconstrictor response to tyramine was abolished after reserpine treatment, but the responses to noradrenaline (NA) and ATP were not significantly modified. 3. The PNS-induced second peak vasoconstrictor responses were markedly reduced in reserpinized vessels, whereas the first peak vasoconstrictor responses were not so strongly influenced (i.e. they were not significantly affected at 1 Hz, but were significantly affected at 4 and 10 Hz). 4. All reserpine-resistant responses were unaffected by treatment with prazosin, but were abolished by subsequent application of alpha,beta-methylene ATP. The exposure of reserpine-treated tissues to NA almost completely restored tyramine-induced vasoconstriction and the second neurogenic peak vasoconstrictor response, but failed to affect the first neurogenic response. 5. The present results indicate that ATP and NA are cotransmitters responsible for the double-peaked vasoconstrictor responses of canine splenic artery. In addition, it is suggested that PNS causes NA release not only from intragranular NA storage sites, but also from tyramine-sensitive cytoplasmic sites.