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Concerning the nature of the histamine-antagonistic effect of adrenaline in the pulmonary circulation

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Summary

In guinea pig heart-lung-preparations histamine provoked an increase of the pulmonary vascular resistance with corresponding increase of the pulmonary artery pressure.

Administration of adrenaline prior to histamine prevented the histamine effect completely. Isoproterenol acted like adrenaline, noradrenaline was ineffective.

Adrenaline by its own had no relaxing effect on the pulmonary vessels but even increased the vascular resistance. In contrast, isoproterenol decreased the vascular resistance.

The β-blocking agent propranolol prevented the histamine-antagonistic adrenaline and isoproterenol effect, and increased the histamine effect on the pulmonary vessels. The α-blocking drug dibenamine did not inhibit the antispastic effect of adrenaline nor the spastic effect of histamine.

The increase of the pulmonary vascular resistance provoked by adrenaline was enhanced by propranolol and abolished by dibenamine. The decrease of the resistance provoked by isoproterenol was blocked by propranolol.

According to these observations, adrenaline antagonizes the spastic histamine effect on the pulmonary vessels by a mechanism involving stimulation of β-adrenergic receptors. The concurrent increasing effect of adrenaline on the vascular resistance is presumably due to α-adrenergic stimulation.

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Authors and Affiliations

  1. Pharmakologisches Institut der Universität Freiburg i. Br., Freiburg i. Br., Germany

    W. Bernauer & G. Brandenbusch

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  1. W. Bernauer
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  2. G. Brandenbusch
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Bernauer, W., Brandenbusch, G. Concerning the nature of the histamine-antagonistic effect of adrenaline in the pulmonary circulation. Naunyn-Schmiedeberg's Arch. Pharmacol. 272, 325–335 (1972). https://doi.org/10.1007/BF00499043

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  • DOI: https://doi.org/10.1007/BF00499043

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