Expression of kinin B1 receptor in fresh or cultured rabbit aortic smooth muscle: role of NF-κB

Kinin B 1 receptor (B 1 R) expression and the importance of the transcription factor nuclear factor (NF)-κB 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-1β, 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-κB (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-κB 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.