Mechanisms of the ergonovine-induced vasoconstriction in the rabbit main coronary artery

Akiko Chishaki, Hirosi Kuriyama

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The mean membrane potential of smooth muscle cells of the rabbit main coronary artery was-60.3 mV and an evoked action potential could be recorded in response to acetylcholine (ACh). Ergonovine or 5-hydroxytryptamine (5-HT) slightly depolarized the membrane and methysergide, a relatively selective antagonist for the 5-HT receptor, had a slight inhibitory action on these depolarizations. 5-HT produced larger contractions than ergonovine, and the concentration-effect relationships obtained for both agents shifted to higher concentrations following pre-equilibration with methysergide. ACh (10-11 M) slightly hyperpolarized the membrane and relaxed the tissue, and high concentrations of ACh (>10-8 M) depolarized the membrane, increased the membrane resistance and produced a contraction. ACh but not ergonovine or 5-HT, produced a contraction in Ca-free EGTA-containing solution. Following a 60 min pre-equilibration with indomethacin, the ergonovine-induced contraction was markedly enhanced but the 5-HT-or ACh-induced contractions were not. Removal of the endothelium by rubbing the vascular lumen enhanced the ergonovine-or ACh-induced contractions, but not those to 5-HT. The results obtained can be summarized as follows: ergonovine probably accelerates Ca influx and thereby produces contraction in the rabbit main coronary artery. This contraction is due to activation of the 5-HT receptor as an agonist, but the ergonovine-induced contraction is attenuated due to activation of the endothelium from which inhibitory prostanoid substances may be released. Ergonovine, therefore, may produce greater contractions in coronary arteries with damaged endothelium than in intact tissues.

Original languageEnglish
Pages (from-to)357-363
Number of pages7
JournalNaunyn-Schmiedeberg's Archives of Pharmacology
Volume326
Issue number4
DOIs
Publication statusPublished - Dec 1 1984

Fingerprint

Ergonovine
Vasoconstriction
Coronary Vessels
Acetylcholine
Rabbits
Serotonin
Methysergide
Membranes
Serotonin Receptors
Endothelium
Egtazic Acid
Vascular Endothelium
Evoked Potentials
Indomethacin
Membrane Potentials
Action Potentials
Prostaglandins
Smooth Muscle Myocytes

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

Mechanisms of the ergonovine-induced vasoconstriction in the rabbit main coronary artery. / Chishaki, Akiko; Kuriyama, Hirosi.

In: Naunyn-Schmiedeberg's Archives of Pharmacology, Vol. 326, No. 4, 01.12.1984, p. 357-363.

Research output: Contribution to journalArticle

@article{a12d049028ce4ff8b7a83ba8d36bd3e0,
title = "Mechanisms of the ergonovine-induced vasoconstriction in the rabbit main coronary artery",
abstract = "The mean membrane potential of smooth muscle cells of the rabbit main coronary artery was-60.3 mV and an evoked action potential could be recorded in response to acetylcholine (ACh). Ergonovine or 5-hydroxytryptamine (5-HT) slightly depolarized the membrane and methysergide, a relatively selective antagonist for the 5-HT receptor, had a slight inhibitory action on these depolarizations. 5-HT produced larger contractions than ergonovine, and the concentration-effect relationships obtained for both agents shifted to higher concentrations following pre-equilibration with methysergide. ACh (10-11 M) slightly hyperpolarized the membrane and relaxed the tissue, and high concentrations of ACh (>10-8 M) depolarized the membrane, increased the membrane resistance and produced a contraction. ACh but not ergonovine or 5-HT, produced a contraction in Ca-free EGTA-containing solution. Following a 60 min pre-equilibration with indomethacin, the ergonovine-induced contraction was markedly enhanced but the 5-HT-or ACh-induced contractions were not. Removal of the endothelium by rubbing the vascular lumen enhanced the ergonovine-or ACh-induced contractions, but not those to 5-HT. The results obtained can be summarized as follows: ergonovine probably accelerates Ca influx and thereby produces contraction in the rabbit main coronary artery. This contraction is due to activation of the 5-HT receptor as an agonist, but the ergonovine-induced contraction is attenuated due to activation of the endothelium from which inhibitory prostanoid substances may be released. Ergonovine, therefore, may produce greater contractions in coronary arteries with damaged endothelium than in intact tissues.",
author = "Akiko Chishaki and Hirosi Kuriyama",
year = "1984",
month = "12",
day = "1",
doi = "10.1007/BF00501443",
language = "English",
volume = "326",
pages = "357--363",
journal = "Naunyn-Schmiedeberg's Archives of Pharmacology",
issn = "0028-1298",
publisher = "Springer Verlag",
number = "4",

}

TY - JOUR

T1 - Mechanisms of the ergonovine-induced vasoconstriction in the rabbit main coronary artery

AU - Chishaki, Akiko

AU - Kuriyama, Hirosi

PY - 1984/12/1

Y1 - 1984/12/1

N2 - The mean membrane potential of smooth muscle cells of the rabbit main coronary artery was-60.3 mV and an evoked action potential could be recorded in response to acetylcholine (ACh). Ergonovine or 5-hydroxytryptamine (5-HT) slightly depolarized the membrane and methysergide, a relatively selective antagonist for the 5-HT receptor, had a slight inhibitory action on these depolarizations. 5-HT produced larger contractions than ergonovine, and the concentration-effect relationships obtained for both agents shifted to higher concentrations following pre-equilibration with methysergide. ACh (10-11 M) slightly hyperpolarized the membrane and relaxed the tissue, and high concentrations of ACh (>10-8 M) depolarized the membrane, increased the membrane resistance and produced a contraction. ACh but not ergonovine or 5-HT, produced a contraction in Ca-free EGTA-containing solution. Following a 60 min pre-equilibration with indomethacin, the ergonovine-induced contraction was markedly enhanced but the 5-HT-or ACh-induced contractions were not. Removal of the endothelium by rubbing the vascular lumen enhanced the ergonovine-or ACh-induced contractions, but not those to 5-HT. The results obtained can be summarized as follows: ergonovine probably accelerates Ca influx and thereby produces contraction in the rabbit main coronary artery. This contraction is due to activation of the 5-HT receptor as an agonist, but the ergonovine-induced contraction is attenuated due to activation of the endothelium from which inhibitory prostanoid substances may be released. Ergonovine, therefore, may produce greater contractions in coronary arteries with damaged endothelium than in intact tissues.

AB - The mean membrane potential of smooth muscle cells of the rabbit main coronary artery was-60.3 mV and an evoked action potential could be recorded in response to acetylcholine (ACh). Ergonovine or 5-hydroxytryptamine (5-HT) slightly depolarized the membrane and methysergide, a relatively selective antagonist for the 5-HT receptor, had a slight inhibitory action on these depolarizations. 5-HT produced larger contractions than ergonovine, and the concentration-effect relationships obtained for both agents shifted to higher concentrations following pre-equilibration with methysergide. ACh (10-11 M) slightly hyperpolarized the membrane and relaxed the tissue, and high concentrations of ACh (>10-8 M) depolarized the membrane, increased the membrane resistance and produced a contraction. ACh but not ergonovine or 5-HT, produced a contraction in Ca-free EGTA-containing solution. Following a 60 min pre-equilibration with indomethacin, the ergonovine-induced contraction was markedly enhanced but the 5-HT-or ACh-induced contractions were not. Removal of the endothelium by rubbing the vascular lumen enhanced the ergonovine-or ACh-induced contractions, but not those to 5-HT. The results obtained can be summarized as follows: ergonovine probably accelerates Ca influx and thereby produces contraction in the rabbit main coronary artery. This contraction is due to activation of the 5-HT receptor as an agonist, but the ergonovine-induced contraction is attenuated due to activation of the endothelium from which inhibitory prostanoid substances may be released. Ergonovine, therefore, may produce greater contractions in coronary arteries with damaged endothelium than in intact tissues.

UR - http://www.scopus.com/inward/record.url?scp=0021264846&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021264846&partnerID=8YFLogxK

U2 - 10.1007/BF00501443

DO - 10.1007/BF00501443

M3 - Article

VL - 326

SP - 357

EP - 363

JO - Naunyn-Schmiedeberg's Archives of Pharmacology

JF - Naunyn-Schmiedeberg's Archives of Pharmacology

SN - 0028-1298

IS - 4

ER -