Membrane electrical mechanism of basilar artery constriction and pial artery dilation by norepinephrine.
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.
D000818:Animals; D001488:Basilar Artery / Q000187:drug effects* / Q000502:physiology; D001921:Brain / Q000098:blood supply*; D002415:Cats; D004305:Dose-Response Relationship, Drug; D008564:Membrane Potentials / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology*; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*
D013757:Tetraethylammonium Compounds; D009638:Norepinephrine