Abstract
The periarterial electrical nerve stimulation at a frequency of 4 Hz (30-s trains of pulses) induced a double-peaked vasoconstriction in the canine splenic artery. The treatment with chloroethylclonidine (CEC, 60 μM) markedly inhibited the second-peaked constriction, whereas it produced an insignificant effect on the first-peaked response. The vasoconstriction to noradrenaline (NA, 1 nmol) was not significantly influenced by 60 μM CEC. On the other hand, WB 4101 (1 μM) consistently abolished the vascular response induced by NA (1 nmol), but rather potentiated the double-peaked constriction. The results indicate that neuronal NA may junctionally exert its vasoconstrictor effect via an activation of postjunctional α1B-receptors, whereas exogenous NA may extrajunctionally activate α1A-receptors for its vascular action in the canine splenic artery.
