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Adrenergic transmissions in the guinea‐pig mesenteric artery and their cholinergic modulations.
Author(s) -
Kuriyama H,
Suzuki H
Publication year - 1981
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1981.sp013831
Subject(s) - acetylcholine , excitatory postsynaptic potential , neuromuscular transmission , muscarinic acetylcholine receptor , stimulation , membrane potential , chemistry , neuromuscular junction , atropine , cholinergic , endocrinology , medicine , anatomy , biophysics , biology , receptor , neuroscience
1. Neuromuscular transmission in the guinea‐pig mesenteric artery and the effect of acetylcholine (ACh) on transmission were investigated by the micro‐electrode method. 2. The membrane potential, length and time constant of the smooth muscle of the mesenteric artery were found to be ‐69.6 +/‐ 1.9 mV, 0.81 +/‐ 0.15 mm and 129 +/‐ 42 msec, respectively. 3. Perivascular nerve stimulation produced an excitatory junction potential (e.j.p.) and repetitive stimulation produced facilitation. When the amplitude of an e.j.p. reached threshold, a spike was evoked. 4. Very rarely, miniature e.j.p.s. were recorded. The amplitude histogram showed a skew distribution. Increases in the stimulus intensity enlarged the amplitude of e.j.p.s. as a stepwise manner. These results indicate multiple innervation to the muscle cells. 5. The time constant of the falling phase of an e.j.p. was consistently larger than that of the muscle membrane. 6. ACh, in concentrations of less than 10(‐8) M, suppressed the e.j.p. amplitude without change in the membrane potential and resistance of the muscle membrane, but accelerated facilitation. These ACh actions were suppressed by pre‐treatment with atropine. 7. ACh suppressed neither the conduction velocity of excitation of adrenergic nerves nor the number of nerves contributing to the generation of an e.j.p. 8. These results suggest that pre‐ and post‐junctional muscarinic receptors possess different sensitivities to ACh, and a low concentration of ACh (less than 10(‐8)M solely suppressed the release of noradrenaline by activating the pre‐junctional muscarinic receptors.