To study the mechanism by which norepinephrine acts on vascular muscle cell membrane, we recorded membrane potential with intracellular microelectrodes in isolated cat basilar and pial arteries. On addition of norepinephrine concentrations less than 1 microM, pial arteries hyperpolarized and relaxed while basilar arteries depolarized and contracted. Relaxation and hyperpolarization of the pial arteries occurred without the need for addition of any other drug, which indicates the relaxation of spontaneous tone. The relaxation and hyperpolarization could be completely blocked by addition of propranolol before exposure to norepinephrine. The depolarization and contraction of both basilar and pial arteries was blocked by the previous exposure to phentolamine. Electrical spikes were not found spontaneously, but could be induced in both arteries by tetraethylammonium and subsequent addition of norepinephrine, blockable by phentolamine. We conclude that membrane property differences between basilar and pial arteries result in qualitatively different effects of norepinephrine.

SUMMARY 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 Ba 2+, a more rapid rate of relaxation from a Ba 2+ contracture, and partial depolarization of the myovascular cells. All of these changes except the quicker relaxation from Ba 2+ 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 trophic 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 Ba 2+ 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 Ba 2+, and thus possible desensitization of noradrenergic receptors. The data thus support a trophic role for NE in the rat portal vein.