Expression of kinin B(1) receptor in fresh or cultured rabbit aortic smooth muscle: role of NF-kappa B.

Kinin B(1) receptor (B(1)R) expression and the importance of the transcription factor nuclear factor (NF)-kappa B in this process were evaluated in models based on the rabbit aorta: freshly isolated tissue (postisolation induction) and cultured smooth muscle cells (SMCs). A 3-h incubation of freshly isolated tissues determined a sharp B(1)R mRNA increase (RT-PCR). Coincubation of tissues with a stimulus (interleukin-1 beta, fetal bovine serum, epidermal growth factor, or cycloheximide) further increased mRNA levels. Cultured SMCs possessed a basal population of surface B(1)Rs ([(3)H]Lys-des-Arg(9)-bradykinin binding) that was upregulated by treatments with the same set of stimuli (binding, mRNA, nuclear runon). Pharmacological inhibitors of NF-kappa B (MG-132, BAY 11-7082, dexamethasone) or actinomycin D reduced the postisolation induction of B(1)Rs in fresh aortic tissue (contractility or mRNA) and the cytokine effect on cells (mRNA, binding). NF-kappa B may be a common mediator of various stimuli that increase B(1)R gene transcription in the rabbit aorta, including tissue isolation, but cycloheximide also stabilizes B(1)R mRNA. The SMC models faithfully mimic the in vivo situation with regard to B(1)R regulation.