MEMBRANE PROPERTIES AND EXCITATORY NEUROMUSCULAR TRANSMISSION IN THE SMOOTH MUSCLE OF DOG CEREBRAL ARTERIES

MEMBRANE PROPERTIES AND EXCITATORY NEUROMUSCULAR TRANSMISSION IN THE SMOOTH MUSCLE OF DOG... 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 (10−5m) 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 × 10−7 m), while phentolamine (10−7m) and yohimbine (10−7m) enhanced the amplitude of e.j.ps. ATP (10−5 m) and noradrenaline (10−6 m) supressed 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png British Journal of Pharmacology Wiley

MEMBRANE PROPERTIES AND EXCITATORY NEUROMUSCULAR TRANSMISSION IN THE SMOOTH MUSCLE OF DOG CEREBRAL ARTERIES

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Publisher
Wiley
Copyright
1982 British Pharmacological Society
ISSN
0007-1188
eISSN
1476-5381
DOI
10.1111/j.1476-5381.1982.tb09286.x
Publisher site
See Article on Publisher Site

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 (10−5m) 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 × 10−7 m), while phentolamine (10−7m) and yohimbine (10−7m) enhanced the amplitude of e.j.ps. ATP (10−5 m) and noradrenaline (10−6 m) supressed 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.

Journal

British Journal of PharmacologyWiley

Published: Oct 1, 1982

References

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