Abstract
Histamine-induced endothelium-dependent relaxation (EDR) in the pulmonary artery was inhibited in a concentration-dependent manner by the phorbolester phorbol 12,13-dibutyrate (PDBu) (IC 50: 70 nM) whereas EDR occurring in response to ionophore A 23187 was not affected by PDBu. The phorbolester 4α-phorbol 12,13-didecanoate (4α-PDD), which does not activate protein kinase C (PKC), was without effect on receptor- or ionophore-induced EDR. The observed inhibition of signal transduction by PKC activation is suggested to reflect phosphorylation of the GTP binding protein N i.
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