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. 1982 Oct;77(2):197–208. doi: 10.1111/j.1476-5381.1982.tb09286.x

Membrane properties and excitatory neuromuscular transmission in the smooth muscle of dog cerebral arteries.

S Fujiwara, T Itoh, H Suzuki
PMCID: PMC2044598  PMID: 6291682

Abstract

1 Drug actions on electrical and mechanical properties of smooth muscle cells and neuromuscular transmission in the canine cerebral arteries were investigated by use of microelectrode and isometric tension recording methods. 2 In the basilar and middle cerebral arteries, the resting membrane potentials were--49.4 mV and -51.7 mV, respectively, the length constants 0.57 mm and 0.45 mm, respectively and the time constants 142 ms and 118 ms, respectively. 3 Outward current pulses did not evoke the spike in either artery but did evoke the spike under conditions of pretreatment with 10 mM tetraethylammonium (TEA). 4 The maximum slope of depolarization produced by a ten fold increase in [K]o plotted on a log scale was 40.1 mV in the basilar artery and 42.2 mV in the middle cerebral artery. 2-Nicotinamidoethyl nitrate, the K-permeability accelerator, had no effect on the membrane potential. 5 K-free or ouabain [10(-5)M] treatment slightly depolarized the membrane. Re-addition of K [5.9 mM] hyperpolarized the membrane by several mV. Thus, the contribution of an active Na-K pump in the membrane potential seems to be small. 6 In both arteries, acetylcholine, adenosine, noradrenaline and isoprenaline in concentrations up to 10(-5)M did not modify the membrane potential and resistance, while 5-hydroxytryptamine (over 10(-8)M) and ATP (over 10(-5)M) depolarized the membrane, decreased the membrane resistance and produced a dose-dependent contraction. Adenosine suppressed the contraction evoked by excess [K]o (39.8 mM). 7 Perivascular nerve stimulation produced excitatory junction potentials (e.j.ps). Often e.j.ps were followed by a hyperpolarization. Repetitive stimulation produced facilitation after several stimuli and depression followed. In some cells, this depression appeared without facilitation. 8 The e.j.ps ceased with pretreatment with guanethidine (10(-6)M) or tetrodotoxin (3 X 10(-7)M), while phentolamine (10(-7)M) and yohimbine (10(-7)M) enhanced the amplitude of e.j.ps. ATP (10(-5)M) and noradrenaline (10(-6)M) suppressed and prazosin had little effect on the e.j.ps. Atropine (10(-6)M) also had no effect on the e.j.ps. 9 Specific features of the cerebral artery and systemic vascular beds were compared, and the features of adrenoceptors on the smooth muscle membrane were compared with findings in other vascular beds.

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Selected References

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