Abstract:
:Electrical responses induced by perivasascular nerve stimulation were recorded intracellularly from the smooth muscle of dog middle cerebral artery. With nerve stimulation, the muscle membrane produced excitatory junction potential and then a slow hyperpolarization. The excitatory junction potential showed facilitation and the slow hyperpolarization showed depression phenomena, when the nerves were stimulated with twin pulses. Generation of the slow hyperpolarization was associated with an increase in the potassium conductance of the membrane and was suppressed by tetraethylammonium, which depolarized the membrane, reduced the membrane conductance, and increased the amplitude of the excitatory junction potential. Treatment with 6-hydroxydopamine abolished the excitatory junction potential, but not the slow hyperpolarization; the latter was suppressed by tetrodotoxin. The amplitude of slow hyperpolarization was decreased by application of tetraethylammonium or ATP, but was not affected by application of atropine, neostigmine, theophylline, apamin, ouabain, norepinephrine, propranolol, or guanethidine. ATP produced transient depolarization of the membrane with associated decrease in the membrane resistance. The excitatory junction potential was attributed to activation of the noradrenergic nerves, whereas the slow hyperpolarization was not generated by activation of adrenergic, cholinergic, or purinergic receptors. Inasmuch as the electrogenic Na-K pump, cAMP, and ATP were not involved in the generation of slow hyperpolarization, the possibility of an unidentified chemical transmitter should be given attention.
journal_name
Circ Resjournal_title
Circulation researchauthors
Suzuki H,Fujiwara Sdoi
10.1161/01.res.51.6.751subject
Has Abstractpub_date
1982-12-01 00:00:00pages
751-9issue
6eissn
0009-7330issn
1524-4571journal_volume
51pub_type
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