Morphine and anandamide coupling to nitric oxide stimulates GnRH and CRF release from rat median eminence: neurovascular regulation

Prévot, Vincent; Rialas, Christos M.; Croix, Dominique; Salzet, Michel; Dupouy, Jean‐Paul; Poulain, Pierre; Beauvillain, Jean-Claudé; Stefano, George B.

doi:10.1016/s0006-8993(98)00066-3

Cited by 75 publications

(54 citation statements)

References 55 publications

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“…However, theromin, regardless of concentration, did not stimulate endothelial NO release from human saphenous vein endothelial cells (data not shown). The vein fragments were judged to be in good condition because 1 M morphine released NO (33.6 Ϯ 4.6 nM NO) as expected (38).…”

Section: Discussionmentioning

confidence: 73%

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Theromin, a Novel Leech Thrombin Inhibitor

Salzet¹,

Chopin²,

Baert³

et al. 2000

Journal of Biological Chemistry

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We purified the most potent thrombin inhibitor described to date from the rhynchobdellid leech Theromyzon tessulatum. Designated theromin, it was purified to apparent homogeneity by gel permeation and anion exchange chromatography followed by two reverse-phase steps of high performance liquid chromatography. The primary sequence of theromin (a homodimer of 67 amino acid residues including 16 cysteine residues) was determined by a combination of reduction and s-␤-pyridylethylation, Edman degradation, trypsin enzymatic digestion, and matrix-assisted laser desorption mass spectrometry measurement. Theromin exhibits no sequence homology with any other thrombin inhibitors. Furthermore, theromin significantly diminishes, in a dose-dependent manner, the level of human granulocyte and monocyte activation induced by lipopolysaccharides. In summary, this potent thrombin inhibitor promises to have high biomedical significance.

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Section: Discussionmentioning

confidence: 73%

“…We sought to determine whether theromin could release endotheliumderived nitric oxide (NO) as well (38). However, theromin, regardless of concentration, did not stimulate endothelial NO release from human saphenous vein endothelial cells (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Theromin, a Novel Leech Thrombin Inhibitor

Salzet¹,

Chopin²,

Baert³

et al. 2000

Journal of Biological Chemistry

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“…This anandamide-induced production of NO inhibited the release of norepinephrine from sympathetic nerve endings in the renal artery (Deutsch et al, 1997) demonstrating that anandamide possesses both vasorelaxant and neuromodulatory properties. Similarly, anandamide is also reported to stimulate the production of NO from the vascular endothelium of the rat portal plexus (Prevot et al, 1998). The e ects of CB1 agonists appear to vary with the vascular bed under investigation since none of the CB1 agonists used a ected tone in rabbit carotid or porcine coronary arteries.…”

Section: Discussionmentioning

confidence: 95%

Inhibition of the production of endothelium‐derived hyperpolarizing factor by cannabinoid receptor agonists

Fleming

Schermer

Popp

et al. 1999

British J Pharmacology

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1 The endogenous cannabinoid, anandamide, has been reported to induce an`endothelium-derived hyperpolarizing factor (EDHF)-like' relaxation in vitro. We therefore investigated the e ects of cannabinoid CB1 receptor agonists; HU 210, D 9 -tetrahydrocannabinol (D 9 -THC) and anandamide, and a CB1 antagonist/inverse agonist, SR 141716A, on nitric oxide (NO) and EDHF-mediated relaxation in precontracted rings of porcine coronary, rabbit carotid and mesenteric arteries. 2 In rings of mesenteric artery HU 210 and D 9 -THC induced endothelium-and cyclo-oxygenaseindependent relaxations which were sensitive to SR 141716A. Anandamide (0.03 ± 30 mM) induced a slowly developing, endothelium-independent relaxation which was abolished by diclofenac and was therefore mediated by cyclo-oxygenase product(s). None of the CB1 agonists tested a ected the tone of precontracted rings of rabbit carotid or porcine coronary artery. 3 In endothelium-intact segments, HU 210, D 9 -THC and anandamide did not a ect NO-mediated responses but under conditions of continuous NO synthase/cyclo-oxygenase blockade, signi®cantly inhibited acetylcholine and bradykinin-induced relaxations which are attributed to the production of EDHF. The e ects of HU 210 and D 9 -THC were not observed when experiments were performed in the presence of SR 141716A suggesting the involvement of the CB1 receptor. 4 In a patch clamp bioassay of EDHF production, HU 210 decreased the EDHF-mediated hyperpolarization of detector smooth muscle cells when applied to the donor segment but was without e ect on the membrane potential of detector cells. The inhibition of EDHF production was unrelated to alterations in Ca 2+ -signalling or cytochrome P450 activity. 5 These results suggest that the activation of endothelial CB1 receptors appears to be negatively coupled to the production of EDHF.

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“…Morphinergic signaling involves selective coupling of the 3 opiate receptor to production and release of NO via Ca 2ϩ -stimulated activation of constitutive nitric oxide synthase (cNOS) and appears to integrate autocrine/paracrine regulatory loops within cellular microdomains (20,22). It is our contention that 3 opiate receptor/NO coupled signaling represents a primordial system of intra/intercellular communication that has been functionally conserved via extensive evolutionary adaptation, resulting in the development and elaboration of endogenous opioid peptide systems and their cognate , ␦, and opioid/G-protein coupled receptorlinked transduction pathways.…”

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confidence: 99%

A Functionally Coupled μ3-Like Opiate Receptor/Nitric Oxide Regulatory Pathway in Human Multi-Lineage Progenitor Cells

Cadet

Mantione

Zhu

et al. 2007

The Journal of Immunology

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Ongoing studies from our group support the existence and biological importance of a distinct cellular signaling pathway involving endogenously synthesized, chemically authentic, l-morphine, its cognate μ3 opiate receptor subtype, and constitutive NO synthase. Based on prior studies indicating evolutionary conservation and adaptation of morphinergic/NO-coupled signaling to mediate autocrine/paracrine control of cellular functions, our goal was to determine whether a functionally competent μ3 opiate receptor/NO-coupled regulatory pathway exists in human multilineage progenitor cells (MLPC) prepared from umbilical cord blood. Real-time PCR analysis indicated significant expression of μ3 opiate receptor-encoding RNA by undifferentiated human MLPC, in the absence of traditional μ1 opioid receptor-encoding RNA expression. Unpredictably, confirmatory RT-PCR analyses indicated cellular expression of a splice variant of the previously characterized μ3 opiate receptor-encoding mRNA. Pharmacological analyses provided critical validating evidence of functional μ3-like opiate receptor/NO-coupled signaling within primary cultures of undifferentiated human MLPC via morphine-evoke real-time release of NO. Control analyses indicated that morphine-stimulated NO release was markedly inhibited by prior treatment with the opiate antagonist l-naloxone or the constitutive NO synthase inhibitor N(G)-nitro-l-arginine methyl ester and unresponsive to stimulation by the opioid peptide methionine enkephalin. Complementary microarray analysis demonstrated that traditional μ1, δ, and κ opioid receptor gene expression is not detected in both undifferentiated and differentiated MLPC. Chemical differentiation of MLPC into neuronal progenitor cells effected significant phenotypic expression of a variety of neurally-associated genes. Our data provide compelling evidence in support of both the evolutionary primacy and primordial regulatory role of μ3-like opiate receptor/NO signaling in embryogenesis.

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Morphine and anandamide coupling to nitric oxide stimulates GnRH and CRF release from rat median eminence: neurovascular regulation

Cited by 75 publications

References 55 publications

Theromin, a Novel Leech Thrombin Inhibitor

Theromin, a Novel Leech Thrombin Inhibitor

Inhibition of the production of endothelium‐derived hyperpolarizing factor by cannabinoid receptor agonists

A Functionally Coupled μ3-Like Opiate Receptor/Nitric Oxide Regulatory Pathway in Human Multi-Lineage Progenitor Cells

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