Abstract
In this study we investigated the role of protein kinase C (PKC) in the histamine H1-receptor mediated contraction of guinea-pig parenchymal lung strips. Lung strips contract after administration of the PKC activators phorbol-12-myristate-13-acetate (PMA) and dioctanoylglycerol. Prolonged stimulation (45 min.) with a high concentration of PMA abolished subsequent responses to PMA whereas H1-responses were only partially reduced. Administration of a PKC inhibitor (H-7) also led to an inhibition of H1-responses. Experiments with combined incubations with the PKC inhibitor H-7 and the Ca2+-entry blocker verapamil suggest that the PKC contribution to the response is possibly mediated via regulation of Ca2+ influx.
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