Naunyn-Schmiedeberg's Archives of Pharmacology

, Volume 316, Issue 2, pp 165–171

Postocclusive cutaneous vasodilatation mediated by substance P

  • Fred Lembeck
  • Josef Donnerer

DOI: 10.1007/BF00505312

Cite this article as:
Lembeck, F. & Donnerer, J. Naunyn-Schmiedeberg's Arch. Pharmacol. (1981) 316: 165. doi:10.1007/BF00505312


  1. 1.

    The cutaneous vasodilation following arterial occulusion (“reactive hyperemia”) was studied in the rat hind paw. A peak increase in venous outflow of 200–250% was observed within 1 min after a 3 min occlusion period.

  2. 2.

    Chronic denervation as well as capsaicin pretreatment reduced the postocclusive cutaneous vasodilatation by more than 60% (P<0.01). This demonstrates that the reactive vasodilatation is of neurogenic origin and mediated by small diameter afferent fibres.

  3. 3.

    Reduction of the postocclusive cutaneous vasodilatation after histamine depletion by compound 48/80 indicates the involvement of histamine.

  4. 4.

    Among all neuropeptides known to occur in primary sensory neurones only substance P and vasoactive intestinal polypeptide cause vasodilatation when infused i.a. into the rat paw. In contrast to antidromic sensory nerve stimulation or i.a. substance P infusion, vasoactive intestinal polypeptide does not cause plasma extravasation. The vasodilator potency of vasoactive intestinal polypeptide is about 1/500 of substance P in the rat paw. Therefore only substance P is able to mimic the reactive vasodilatation.

  5. 5.

    It is concluded that the postocclusive cutaneous vasodilatation is caused mainly by the release of substance P from peripheral endings of small diameter nerve fibres. The “axon reflex”, also involving neurogenic vasodilatation, is assumed to be exerted by the same mechanism.


Key words

Reactive hyperemia Substance P Vasoactive intestinal polypeptide Neurotensin Histamine Capsaicin 


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Copyright information

© Springer-Verlag 1981

Authors and Affiliations

  • Fred Lembeck
    • 1
  • Josef Donnerer
    • 1
  1. 1.Pain Research Commission of the Austrian Academy of Sciences and Institute of Experimental and Clinical Pharmacology of the University of GrazGrazAustria

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