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. 1988 Jul;94(3):952–960. doi: 10.1111/j.1476-5381.1988.tb11609.x

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

J Pernow 1, T Kahan 1, J M Lundberg 1
PMCID: PMC1854060  PMID: 3179619

Abstract

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 mgkg-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 less than 0.001). Stimulation at 0.59 Hz caused vasoconstriction in the decentralized but not in the intact gracilis.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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