Neuropeptide Y and reserpine‐resistant vasoconstriction evoked by sympathetic nerve stimulation in the dog skeletal muscle

1 The effects of sympathetic nerve stimulation (evoked by recordings of authentic irregular vasoconstrictor nerve fibre discharge with average frequencies of 0.59, 2.0 and 6.9 Hz) on the perfusion pressure and the overflow of noradrenaline (NA) and neuropeptide Y‐like immunoreactivity (NPY‐LI) were investigated in the blood‐perfused gracilis muscle of the dog in situ. 2 Nerve stimulation in the untreated control group evoked a frequency‐dependent increase in perfusion pressure and overflow of NA. A significant overflow of NPY‐LI was found at the highest frequency only. 3 In a separate group of animals, the sympathetic supply was unilaterally interrupted by preganglionic decentralization before the administration of reserpine (1 mg kg−1 i.v.) 24 h before the experiment. Reserpine reduced the NA content of the intact and decentralized gracilis and gastrocnemius muscle by 98–99%. Reserpine also induced a marked (80%) reduction of the muscular content of NPY‐LI. The depletion of NPY‐LI was, in contrast to that of NA, prevented by the decentralization, suggesting that nerve impulse activity was of primary importance for the reserpine‐induced depletion of NPY‐LI. 4 A slowly developing and long‐lasting perfusion pressure increase was evoked by nerve stimulation, at 2.0 and 6.9 Hz after reserpine treatment. These responses were larger in the decentralized, as compared to the intact gracilis muscle and correlated with the nerve stimulation evoked overflow of NPY‐LI (r = 0.79, P < 0.001). Stimulation at 0.59 Hz caused vasoconstriction in the decentralized but not in the intact gracilis. 5 Administration of α,β‐methylene adenosine triphosphate did not evoke an increase in perfusion pressure in the gracilis muscle of reserpine‐treated animals. 6 In conclusion, a large perfusion pressure increase to sympathetic nerve stimulation occurs in the reserpine‐pretreated skeletal muscle vasculature of the dog in vivo, providing that preganglionic decentralization has been performed. It is suggested that the released NPY‐LI may mediate this vasoconstrictor response.