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Über die durch Sympathicomimetica ausgelöste, neurogene Vasodilatation

Neurogenic vasodilatation caused by sympathomimetic amines

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Summary

The hindlimb of the anesthetized dog was perfused at a constant flow rate. Intravenous administration of noradrenaline, adrenaline, dopamine, cobefrine, phenylephrine, norphenephrine, octopamine, heptaminol, tyramine, metaraminol, DMPP, m-bromophenyloxycholine and acetylcholine (after atropine) induced vasodilatation in the auto- or hetero-perfused limb. This effect was abolished by surgical interruption of the sympathetic innervation. Isoprenaline, N,N′-hexamethylen-bis-noradrenaline, angiotensin, vasopressin, acetylcholine (without atropinization), 5-hydroxytryptamine and histamine did not cause neurogenic vasodilatation.

The magnitude of the vasodilatation (indicated by decreases in the perfusion pressure ranging from 10 to 120 mm Hg) depended both on the sensitivity of the experimental animal and on the dose of the drug; no correlation was found between the systemic pressor and the neurogenic vasodilator effects and even doses of adrenaline and dopamine which caused depressor effects produced vasodilatation, a response which was also observed after intraaortic administration of suitable drugs.

Ergotamine caused neurogenic vasodilatation but subsequently abolished it; for ergotamine different points of action could be shown (the perfused hindlimb, systemic circulation and central nervous system). Reserpine pretreatment, phentolamine, promethazine and pheniramine reduced or abolished the neurogenic vasodilatation, while propranolol, atropine and methsergide exerted no influence.

It is concluded that neurogenic vasodilatation cannot be accounted for solely by stimulation of baroreceptors and it is essentially abolished by surgical or pharmacological suppression of sympathetic function or impairment of the release and uptake mechanisms of nerve terminals; it appears to be initiated by stimulation of α-adrenergic receptors. The results obtained do not favour the participation of acetylcholine, histamine or 5-hydroxytryptamine as chemical mediators of neurogenic vasodilatation.

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Authors and Affiliations

  1. Pharmakologisches Laboratorium der Medizinischen Fakultät Porto, Portugal

    W. Osswald

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  1. W. Osswald
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Über einen Teil der Ergebnisse wurde auf der 31. Tagung der Deutschen Pharmakologischen Gesellschaft (Düsseldorf, 23. bis 26.9.1968) berichtet.

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Osswald, W. Über die durch Sympathicomimetica ausgelöste, neurogene Vasodilatation. Naunyn-Schmiedebergs Arch. Pharmak. 265, 67–80 (1969). https://doi.org/10.1007/BF01417210

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  • DOI: https://doi.org/10.1007/BF01417210

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