[D-Met2,Pro5]enkephalinamide activates cardioinhibitory efferents in anaesthetized dogs.

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[D-Met2,Pro5]enkephalinamide activates cardioinhibitory efferents in anaesthetized dogs. / Inoue, K; Nashan, Björn; Arndt, J O.

in: EUR J PHARMACOL, Jahrgang 110, Nr. 2, 2, 1985, S. 233-239.

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@article{5fde025cf81b4bacafb81923e983a02c,
title = "[D-Met2,Pro5]enkephalinamide activates cardioinhibitory efferents in anaesthetized dogs.",
abstract = "[D-Met2,Pro5]enkephalinamide (DMPEA) strongly activated cardioinhibitory vagal efferents and elicited bradycardia when perfused through the cerebroventricular system of anaesthetized dogs. These effects were concentration-dependent but plateaued at an intraventricular concentration of 200 micrograms/ml. At this maximally effective concentration, the vagal discharge rate was fourfold higher and the heart rate was lowered by 28% compared to the controls. These effects were reversed by naloxone (40 micrograms/ml). There was no significant change in blood pressure. Vagal discharge rate and heart rate correlated closely and inversely with each other with r values ranging between -0.75 and -0.95. Opiate receptors in brain structures bordering the cerebroventricular system are the most likely mediators of the effects of DMPEA. The opiate receptor/endorphin system may therefore play a role in the physiological control of cardiac vagal tone and thus of heart rate.",
author = "K Inoue and Bj{\"o}rn Nashan and Arndt, {J O}",
year = "1985",
language = "Deutsch",
volume = "110",
pages = "233--239",
journal = "EUR J PHARMACOL",
issn = "0014-2999",
publisher = "Elsevier",
number = "2",

}

RIS

TY - JOUR

T1 - [D-Met2,Pro5]enkephalinamide activates cardioinhibitory efferents in anaesthetized dogs.

AU - Inoue, K

AU - Nashan, Björn

AU - Arndt, J O

PY - 1985

Y1 - 1985

N2 - [D-Met2,Pro5]enkephalinamide (DMPEA) strongly activated cardioinhibitory vagal efferents and elicited bradycardia when perfused through the cerebroventricular system of anaesthetized dogs. These effects were concentration-dependent but plateaued at an intraventricular concentration of 200 micrograms/ml. At this maximally effective concentration, the vagal discharge rate was fourfold higher and the heart rate was lowered by 28% compared to the controls. These effects were reversed by naloxone (40 micrograms/ml). There was no significant change in blood pressure. Vagal discharge rate and heart rate correlated closely and inversely with each other with r values ranging between -0.75 and -0.95. Opiate receptors in brain structures bordering the cerebroventricular system are the most likely mediators of the effects of DMPEA. The opiate receptor/endorphin system may therefore play a role in the physiological control of cardiac vagal tone and thus of heart rate.

AB - [D-Met2,Pro5]enkephalinamide (DMPEA) strongly activated cardioinhibitory vagal efferents and elicited bradycardia when perfused through the cerebroventricular system of anaesthetized dogs. These effects were concentration-dependent but plateaued at an intraventricular concentration of 200 micrograms/ml. At this maximally effective concentration, the vagal discharge rate was fourfold higher and the heart rate was lowered by 28% compared to the controls. These effects were reversed by naloxone (40 micrograms/ml). There was no significant change in blood pressure. Vagal discharge rate and heart rate correlated closely and inversely with each other with r values ranging between -0.75 and -0.95. Opiate receptors in brain structures bordering the cerebroventricular system are the most likely mediators of the effects of DMPEA. The opiate receptor/endorphin system may therefore play a role in the physiological control of cardiac vagal tone and thus of heart rate.

M3 - SCORING: Zeitschriftenaufsatz

VL - 110

SP - 233

EP - 239

JO - EUR J PHARMACOL

JF - EUR J PHARMACOL

SN - 0014-2999

IS - 2

M1 - 2

ER -