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Possibilities for a cholinergic action on smooth musculature and on sympathetic axons in brain vessels mediated by muscarinic and nicotinic receptors.
J Pharmacol Exp Ther. 1977 Jan; 200(1):117-26.JP

Abstract

A pharmacological identification and characterization of cholinergic receptors was carried out in pial arteries of cats. In one series of experiments, the middle cerebral artery was suspended in an organ bath for recording fo circular motor activity. Parasympathomimetic compounds produced either a relaxation or a contraction. The relaxation occurred at low doses (up to 10(-6) M), and the response was inhibited in a competitive manner by atropine. The mean KB value (determined with acetylcholine as agonist) was 3.85 X 10(-11) M, and the corresponding pA2 value 10.43. At higher doses, the parasympathomimetics produced a contraction. This effect, too, was inhibited in a competitive manner with atropine. The calculated mean KB value with acetylcholine as agonist was 1.12 X 10(-11) M, and pA2 was 10.07. The motor responses did not require an intact perivascular sympathetic innervation, which shows that the effects were mediated by muscarinic type of cholinergic receptors present in the smooth musculature. In another series of experiments, pial arteries were preincubated in the presence of 3H-norepinephrine, and the amount of tritium efflux was measured in a superfusion system before or during electrical field stimulation (12 V, 1 msec pulse duration, 10 Hz). The efflux was minimized by sympathetic denervation, and the effect of transmural stimulation abolished by bretylium and guanethidine, which shows that the bulk of tritium overflow during stimulation originated from the perivascular sympathetic nerves. The marked elevation of tritium efflux during stimulation was enhanced by hexamethonium, and it was inhibited by nicotine and acetylcholine, whose effects were counteracted by hexamethonium (but not by atropine). This finding indicates the presence of nicotinic type of cholinergic receptors on the perivascular adrenergic nerves, allowing inhibition of norepinephrine by acetylcholine that may be liberated from the adjacent cholinergic terminals in the autonomic nerve plexus.

Authors

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Pub Type(s)

Journal Article

Language

eng

PubMed ID

833753

Citation

Edvinsson, L, et al. "Possibilities for a Cholinergic Action On Smooth Musculature and On Sympathetic Axons in Brain Vessels Mediated By Muscarinic and Nicotinic Receptors." The Journal of Pharmacology and Experimental Therapeutics, vol. 200, no. 1, 1977, pp. 117-26.
Edvinsson L, Falck B, Owman C. Possibilities for a cholinergic action on smooth musculature and on sympathetic axons in brain vessels mediated by muscarinic and nicotinic receptors. J Pharmacol Exp Ther. 1977;200(1):117-26.
Edvinsson, L., Falck, B., & Owman, C. (1977). Possibilities for a cholinergic action on smooth musculature and on sympathetic axons in brain vessels mediated by muscarinic and nicotinic receptors. The Journal of Pharmacology and Experimental Therapeutics, 200(1), 117-26.
Edvinsson L, Falck B, Owman C. Possibilities for a Cholinergic Action On Smooth Musculature and On Sympathetic Axons in Brain Vessels Mediated By Muscarinic and Nicotinic Receptors. J Pharmacol Exp Ther. 1977;200(1):117-26. PubMed PMID: 833753.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Possibilities for a cholinergic action on smooth musculature and on sympathetic axons in brain vessels mediated by muscarinic and nicotinic receptors. AU - Edvinsson,L, AU - Falck,B, AU - Owman,C, PY - 1977/1/1/pubmed PY - 1977/1/1/medline PY - 1977/1/1/entrez SP - 117 EP - 26 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 200 IS - 1 N2 - A pharmacological identification and characterization of cholinergic receptors was carried out in pial arteries of cats. In one series of experiments, the middle cerebral artery was suspended in an organ bath for recording fo circular motor activity. Parasympathomimetic compounds produced either a relaxation or a contraction. The relaxation occurred at low doses (up to 10(-6) M), and the response was inhibited in a competitive manner by atropine. The mean KB value (determined with acetylcholine as agonist) was 3.85 X 10(-11) M, and the corresponding pA2 value 10.43. At higher doses, the parasympathomimetics produced a contraction. This effect, too, was inhibited in a competitive manner with atropine. The calculated mean KB value with acetylcholine as agonist was 1.12 X 10(-11) M, and pA2 was 10.07. The motor responses did not require an intact perivascular sympathetic innervation, which shows that the effects were mediated by muscarinic type of cholinergic receptors present in the smooth musculature. In another series of experiments, pial arteries were preincubated in the presence of 3H-norepinephrine, and the amount of tritium efflux was measured in a superfusion system before or during electrical field stimulation (12 V, 1 msec pulse duration, 10 Hz). The efflux was minimized by sympathetic denervation, and the effect of transmural stimulation abolished by bretylium and guanethidine, which shows that the bulk of tritium overflow during stimulation originated from the perivascular sympathetic nerves. The marked elevation of tritium efflux during stimulation was enhanced by hexamethonium, and it was inhibited by nicotine and acetylcholine, whose effects were counteracted by hexamethonium (but not by atropine). This finding indicates the presence of nicotinic type of cholinergic receptors on the perivascular adrenergic nerves, allowing inhibition of norepinephrine by acetylcholine that may be liberated from the adjacent cholinergic terminals in the autonomic nerve plexus. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/833753/Possibilities_for_a_cholinergic_action_on_smooth_musculature_and_on_sympathetic_axons_in_brain_vessels_mediated_by_muscarinic_and_nicotinic_receptors_ L2 - http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=833753 DB - PRIME DP - Unbound Medicine ER -