[Met5]enkephalin-Arg-Phe acts on vascular opiate receptors

Rónai, András Z.; Hársing, LászlóG G.; Berzétei, I.; Bajusz, S.; Vizi, E. Sylvester

doi:10.1016/0014-2999(82)90645-8

Cited by 28 publications

(7 citation statements)

References 4 publications

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“…There are reports that in the perfused rabbit ear artery, EKC (Ronai et al, 1982), [Met]enkephalin (Knoll, 1976;Ronai et al, 1982) and [Leu]enkephalin (Illes et al, 1983) (Hanko & Hardebo, 1978). In contrast to the finding of Ronai et al (1982) that EKC caused full inhibition, we found that EKC produced only partial inhibition.…”

Section: Effects Ofopioids On Vascular Smooth Musclecontrasting

confidence: 99%

“…In contrast to the finding of Ronai et al (1982) that EKC caused full inhibition, we found that EKC produced only partial inhibition. This discrepancy may be due to differences in the experimental conditions.…”

Section: Effects Ofopioids On Vascular Smooth Musclecontrasting

confidence: 99%

“…by the findings that enkephalins act on neuronal opioid receptors in the perfused rabbit ear artery (Knoll, 1976;Ronai et al, 1982;Illes et al, 1983), and on opioid receptors in the vessel walls (Hanko & Hardebo, 1978;Altura et al, 1980). In addition to the enkephalins, opioids such as morphine and bremazocine have been shown to cause vasodilatation both in vivo (Altura et al, 1980) and in vitro (Hanko & Hardebo, 1978) via specific postsynaptic opioid receptors in vascular smooth muscle.…”

Section: Introductionmentioning

confidence: 99%

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Opioid receptor types on adrenergic nerve terminals of rabbit ear artery

Fukuda¹,

Hosoki²,

Ishida³

et al. 1985

British J Pharmacology

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1 Methionine enkephalin, leucine enkephalin, enkephalin, a-neoendorphin, fendorphin, dynorphin (I -13) and ethylketocyclazocine inhibited the contractions of rabbit ear artery ring segments elicited by transmural nerve stimulation at 8 Hz. 2 Ethylketocyclazocine, dynorphin (1-13) and leucine enkephalin produced partial inhibition, their apparent intrinsic activities (a) being 0.57, 0.75 and 0.66, respectively.3 Morphine and normorphine, which are agonists at ji-receptors, did not inhibit the response of the artery.4 Naloxone antagonized the actions of opioids and ethylketocyclazocine, and was more effective against methionine enkephalin, leucine enkephalin and [D-Ala2, D-Leu5] enkephalin than against aneoendorphin, ethylketocyclazocine and dynorphin (I-13). The pA2 values of naloxone against socalled 6-agonists were approx. 8.5, and against so-called K-agonists were approx. 7.7. 5 The supposed K-antagonist, Mr 2266, was more effective than naloxone in antagonizing the actions of a-neoendorphin, and the ic-agonists dynorphin (1-13) and ethylketocyclazocine. The pA2 values of Mr 2266 against ic-agonists were 8.5-9.0, and against 6-agonists were 7.8 or less. 6 The opioid peptides and opioids tested did not cause dilatation of the artery previously contracted with histamine. 7 These results suggest that the opioid peptides and ethylketocyclazocine acted on opioid receptors at adrenergic nerve terminals in the ear artery.8 The opioid receptors appear to be of the 6-and K-types, not the it-type.

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Section: Effects Ofopioids On Vascular Smooth Musclecontrasting

confidence: 99%

Section: Effects Ofopioids On Vascular Smooth Musclecontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Opioid receptor types on adrenergic nerve terminals of rabbit ear artery

Fukuda¹,

Hosoki²,

Ishida³

et al. 1985

British J Pharmacology

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“…With respect to their presence together with catecholamines, the possible mode of action of enkephalins may be either an interaction with noradrenaline or an independent, direct effect on the blood vessels. A number of physiological and pharmacological studies suggests that both possibilities may occur [4], For exam ple, the electrically induced neurogenic va soconstriction of the perfused rabbit ear ar tery was found to be markedly inhibited by both Leu-and Met-enkephalin, whose effect was antagonized by naloxone and naltrex one [79,80], Since the vasoconstrictor re sponse to noradrenaline remained un changed in the presence of enkephalins at concentrations blocking the response to nerve stimulation, the effect was interpreted as being prejunctional. This assumption has been supported in studies of radioactive transmitter overflow during electrical nerve stimulation, including blockade with nalox one [81].…”

Section: Enkephalinsmentioning

confidence: 99%

Peptidergic Vasodilator Nerves in the Peripheral Circulation and in the Vascular Beds of the Heart and Brain

Owman

1990

J Vasc Res

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This overview focusses on the ubiquitous presence of immunohistochemically visible peptidergic nerves with vasodilatory function. The nerve fibres are primarily related to the parasympathetic system (vasoactive intestinal polypeptide or VIP), the sympathetic system including the adrenal medulla (enkephalins) and to the sensory system (substance P as well as calcitonin gene-related peptide, CGRP). Substance P and probably also CGRP seem to be the mediators of antidromic vasodilatation. Enkephalins appear to be released both from nerve endings and from the adrenomeduUary cells. The vasodilatory nerve fibres in the heart distribute both to the coronary vessels and to functionally important parts of the myocardium, where interesting relations exist between the peptidergic flow regulation and contractile force. In the brain the sensory and parasympathetic pathways for VIP and substance P/CGRP have recently been mapped in detail, and a new peptidergic intracranial ganglion has been discovered. The selective electrical stimulation of the sensory and post-ganglionic parasympathetic fibres, respectively, in the brain circulation has been found to evoke a pronounced flow increase which does not appear to involve cholinergic mediation. There is also experimental evidence that the mentioned systems of fibres may interact with each other and with the sympathetic nervous system by way of neuronal cross-talk.

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“…the activation of inhibitory receptors situated at post-ganglionic sympathetic nerve terminals in blood vessels, may be also involved in the hypotensive effect of opioids (Illes & Pfeiffer, 1985). The presence of such presynaptic receptors (Starke, 1977;Henderson, Hughes & Kosterlitz, 1979) has been demonstrated in the rabbit ear artery (Knoll, 1976;Ronai, Harsing, Berzetei, Bajusz & Vizi, 1982;Illes, Pfeiffer, von Kilgelgen & Starke, 1985a) and ileocolic artery (von Kilgelgen, Illes, Wolf & Starke, 1985). Except in some cerebral arteries (Hanko & Hardebo, 1978;Altura, Altura & Quirion, 1984;Harder & Madden, 1984) opioids do not cause vasodilation by a direct effect on the smooth muscle, although they may attenuate noradrenalineinduced vasoconstriction (Ruth, Doerr & Eiden, 1984).…”

Section: Introductionmentioning

confidence: 99%

Presynaptic opioid delta‐receptors in the rabbit mesenteric artery.

Illéš¹,

Ramme²,

Starke³

1986

The Journal of Physiology

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Excitatory junction potentials (e.j.p.s) evoked by nerve stimulation were recorded from muscle cells of the rabbit isolated mesenteric artery. At 0.03 Hz the e.j.p. amplitudes were stable. When a train of fifteen pulses was applied at 0.25 Hz or at higher frequencies (0.5, 1 and 2 Hz), e.j.p.s showed an initial facilitation followed by depression. [Met5]enkephalin 0.1 and 1 mumol/l, [D‐Ala2,D‐Leu5]enkephalin 0.1 and 1, but not 0.01 mumol/l, and [D‐Pen2, L‐Pen5]enkephalin 3 mumol/l all depressed the e.j.p.s evoked by trains of fifteen pulses at 1 Hz. When more than one concentration was used ([Met5]enkephalin, [D‐Ala2,D‐Leu5]enkephalin), the inhibition was concentration dependent. It was always greater for the first few e.j.p.s than for the later ones in a train. [Met5]enkephalin 1 mumol/l reduced the first e.j.p. at 1 Hz and the e.j.p.s evoked by 0.03 Hz to a similar extent. The inhibitory effect of [Met5]enkephalin 1 mumol/l on e.j.p.s persisted in the presence of yohimbine 0.3 mumol/l. Naloxone 1 mumol/l did not interfere with the effect of [Met5]enkephalin 1 mumol/l. Naloxone 10 mumol/l depressed some e.j.p.s and prevented the inhibition by [Met5]enkephalin 1 mumol/l. Neither ICI 154129 10 mumol/l nor ICI 174864 0.3 mumol/l had any effect of their own and both compounds antagonized the action of [Met5]enkephalin 1 mumol/l. Normorphine 10 mumol/l, fentanyl 1 mumol/l, ethylketocyclazocine 0.1 mumol/l, and dynorphin A(1‐13) 1 mumol/l were all ineffective. Ethylketocyclazocine 1 mumol/l did not change the e.j.p.s either, but antagonized [Met5]enkephalin 1 mumol/l. [Met5]enkephalin 1 mumol/l failed to influence both the resting membrane potential of the muscle cells and the depolarizing effect of noradrenaline 3 and 30 mumol/l. We suggest that the axon terminals of post‐ganglionic sympathetic neurones in the rabbit mesenteric artery possess opioid delta‐, but not mu‐ or kappa‐receptors. The activation of presynaptic delta‐receptors inhibits the release of the neuroeffector transmitter. There is no evidence for any effect of co‐released endogenous opioid peptides under our experimental conditions.

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[Met5]enkephalin-Arg-Phe acts on vascular opiate receptors

Cited by 28 publications

References 4 publications

Opioid receptor types on adrenergic nerve terminals of rabbit ear artery

Opioid receptor types on adrenergic nerve terminals of rabbit ear artery

Peptidergic Vasodilator Nerves in the Peripheral Circulation and in the Vascular Beds of the Heart and Brain

Presynaptic opioid delta‐receptors in the rabbit mesenteric artery.

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