Inhibition of neurogenic vasodilatation and plasma extravasation by substance P antagonists, somatostatin and [D-Met2, Pro5]enkephalinamide

Fred Lembeck, Josef Donnerer, L. Barthó

Research output: Contribution to journalArticle

212 Citations (Scopus)

Abstract

The substance P (SP) analogues [D-Pro2, D-Phe7, D-Phe7]SP and [D-Pro2, D-Trp7,9]SP, which have been reported to be SP antagonists, inhibited the vasodilatation and plasma extravasation induced by antidromic stimulation of the saphenous nerve or by i.a. infusion of SP. Somatostatin inhibited the vasodilatation and plasma extravasation induced by saphenous nerve stimulation, but had no effect on the vascular responses to i.a. infused SP. The opiate agonist [D-Met2, Pro5]enkephalinamide inhibited the vasodilatation evoked by antidromic nerve stimulation in a naloxone reversible manner, but did not change the effect of i.a. infusion of SP. Calcitonin and caerulein had no effect on neurogenic vasodilatation. These results further support the concepts that neurogenic vasodilatation and plasma extravasation are mediated by SP, and that somatostatin and opiates inhibit the release of SP from peripheral sensory nerve endings.

Original languageEnglish
Pages (from-to)171-176
Number of pages6
JournalEuropean Journal of Pharmacology
Volume85
Issue number2
DOIs
Publication statusPublished - Nov 19 1982

Fingerprint

Substance P
Somatostatin
Vasodilation
Opiate Alkaloids
Ceruletide
Calcitonin
Sensory Receptor Cells
Naloxone
Peripheral Nerves
Blood Vessels

Keywords

  • Antidromic vasodilatation
  • Neurogenic plasma extravasation
  • Somatostatin
  • Substance P
  • Substance P antagonists
  • [D-Met, Pro]enkephalinamide

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

Inhibition of neurogenic vasodilatation and plasma extravasation by substance P antagonists, somatostatin and [D-Met2, Pro5]enkephalinamide. / Lembeck, Fred; Donnerer, Josef; Barthó, L.

In: European Journal of Pharmacology, Vol. 85, No. 2, 19.11.1982, p. 171-176.

Research output: Contribution to journalArticle

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