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The periarterial electrical nerve stimulation (30 s trains of pulses at a frequency of 1, 4 or 10 Hz) induced a double peaked vasoconstriction consisting of an initial transient constriction (first peak) followed by a prolonged response (second peak) in the isolated, perfused canine splenic artery.At low frequencies (1 and 4 Hz), a neuropeptide Y (NPY) Y1receptor antagonist BIBP 3226 (0.1–1 μM) produced a dose‐dependent inhibitory effect on the second peak, but did not modify the first peak. At a high frequency (10 Hz), 1 μMBIBP 3226 induced a slight, but significant inhibition on both the first and second peaked responses.At a low frequency (1 Hz), the first peak was not influenced by blockade of α1‐adrenoceptors or NPY Y1receptors with prazosin (0.1 μM) or BIBP 3226 (1 μM), respectively, but abolished by P2X receptor desensitization with α,β‐methylene ATP (αβ‐m ATP, 1 μM). At a high frequency (10 Hz), the first peak was mostly inhibited by αβ‐m ATP and partially by prazosin and BIBP 3226. On the other hand, the second peak at a low frequency was largely decreased by BIBP 3226 and partially by prazosin and αβ‐m ATP, whereas at a high frequency, it was largely attenuated by prazosin and partially by αβ‐m ATP and BIBP 3226.The results suggest that at a low frequency, the firstly transient constriction of double peaked responses is mainly induced viaan activation of P2X‐receptors, whereas at a high frequency, it is mostly mediated by the P2X‐receptors, and partially by α1‐receptors and NPY Y1‐receptors. The secondary prolonged vasoconstriction at frequencies used is predominantly mediated viaboth α1‐receptor and NPY Y1receptor activations, and in part by P2X‐receptors. Furthermore, an activation of NPY Y1receptors may play an important role in evoking the prolonged vasoconstrictor response to longer pulse trains of stimulation at a low frequency, whereas an α1‐adrenoceptor activation exerts a main vasomotor effect for the prolonged response at a high frequency.