Guanethidine-sensitive release of neuropeptide Y-like immunoreactivity in the cat spleen by sympathetic nerve stimulation.

Splenic nerve stimulation (10 Hz for 2 min) caused a perfusion-pressure increase, a volume reduction and an increase in the output of neuropeptide Y-like immunoreactivity (NPY-LI) from the isolated blood-perfused cat spleen. Gel-filtration HPLC analysis revealed that plasma NPY-LI collected during nerve stimulation was similar to the NPY-LI in the spleen and synthetic porcine NPY. Combined propranolol and phenoxybenzamine pretreatment enhanced NPY output upon nerve stimulation by about 60%. Forty percent of the perfusion-pressure increase and 25% of the volume reduction seen during control stimulations remained after adrenoceptor blockade. Guanethidine abolished the release of NPY-LI, the perfusion-pressure increase and the volume reduction normally seen upon splenic nerve stimulation. Infusion of synthetic porcine NPY caused a long-lasting increase in perfusion pressure and a relatively moderate volume reduction. Noradrenaline (NA) both increased perfusion pressure and induced a marked volume reduction. The NPY effects were resistant to adrenoceptor antagonists in doses which abolished the NA response. In conclusion, the present data show that NPY-LI is released upon sympathetic nerve stimulation by a guanethidine-sensitive mechanism. Furthermore, the sympathetic response is partially resistant to adrenoceptor antagonists and NPY has powerful vasoconstrictor effects. This provides further evidence for a role of NPY in sympathetic vascular control.