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Rat portal veins were maintained in organ culture to study the development of characteristic denervation changes and a possible trophic effect of the neurotransmitter norepinephrine (NE). Vessels maintained in organ culture for 2 days showed supersensitivity to NE and Ba2+, a more rapid rate of relaxation from a Ba2+ contracture, and partial depolarization of the myovascular cells. All of these changes except the quicker relaxation from Ba2+ contracture could be prevented by incubating the preparations in a NE-containing medium. This evidence suggests that functional changes in vascular muscle cells are caused by the removal of a tropic influence of NE, but can be prevented by NE replacement. However, the failure of NE in the culture media to prevent the increased rate of relaxation from Ba2+ contracture found after 2 days in organ culture suggests that NE is not the only trophic influence acting on the portal vein. In addition, incubation of veins in a NE-containing medium produced a marked subsensitivity to the contractile effects of NE, but not BA2+, and thus possible desensitization of noradrenergic receptors. The data thus support a trophic role for NE in the rat portal vein.

Trophic effect of norepinephrine on the rat portal vein in organ culture.