Inositol 1,4,5-triphosphate and protein kinase C are involved in thrombin- and trap-induced vascular smooth muscle contraction.

Thrombin (30 nmol/l) as well as the thrombin receptor activating peptide (TRAP), 10 mumol/l) induce a sustained contraction of endothelium-denuded porcine pulmonary arteries. The first phasic component of contraction is associated with the generation of IP3 which precedes the development of contractile force. Since the PKC inhibitor staurosporine (50 nmol/l) completely inhibits the tonic contraction this component of contraction seems to be due to the activation of protein kinase C (PKC). The thrombin- and TRAP-induced vasoconstriction strongly depends on extracellular calcium; the remaining thrombin- or TRAP-induced contraction in Ca(2+)-free medium seems to be attributed to the IP3-mediated release of calcium from intracellular stores.