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Bombesin-induced contractions of guinea pig lung strips are modulated by endogenous nitric oxide

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Abstract

We have investigated the effects of a nitric oxide (NO) biosynthesis inhibitor N\sw-nitro-L-arginine methyl ester (l-NAME) on the bombesin-evoked contraction of guinea pig parenchymal lung strips. The bombesin-induced contractions of lung strips were significantly increased after l-NAME (300 μM) pre-treatment. The maximal response was increased (P < 0.01) by 37% after l-NAME treatment when compared with the control group. The pD2 value was not influenced by l-NAME pre-treatment. The enhancement of the bombesin-induced contraction caused by l-NAME was reversed by addition of an excess of the NO precursor-l-arginine (600 μM) but not by the addition of its inactive enantiomer d-arginine (600 μM). Like l-NAME, methylene blue (1 μM), an agent that inhibits the soluble guanylyl cyclase activated by NO, significantly increased (P < 0.01) the maximal contraction induced by bombesin (183 ± 16 mg) when compared with the control group (141 ± 15 mg). When tested against other agonist-induced contractions, l-NAME did not change the responsiveness of parenchymal lung strips to bradykinin or carbachol but significantly increased the lung contraction induced by histamine. NO synthesis inhibition resulted in a pronounced increase in the bombesin-induced contraction of guinea-pig lung strips. Our results suggest that bombesin contributes to NO synthesis and release which then acts to reduce the contraction of the lungstrip in response to bombesin.

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Lach, E., Daefller, L., Waeldele, F. et al. Bombesin-induced contractions of guinea pig lung strips are modulated by endogenous nitric oxide. Naunyn-Schmiedeberg's Arch Pharmacol 352, 419–423 (1995). https://doi.org/10.1007/BF00172779

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