Compounds > enkephalin--ala(2)-mephe(4)-gly(5)-

enkephalin--ala(2)-mephe(4)-gly(5)- and icatibant

enkephalin--ala(2)-mephe(4)-gly(5)- has been researched along with icatibant* in 2 studies

Other Studies

2 other study(ies) available for enkephalin--ala(2)-mephe(4)-gly(5)- and icatibant

Article	Year
Panicolytic-like action of bradykinin in the dorsal periaqueductal gray through μ-opioid and B2-kinin receptors. Neuropharmacology, 2017, Sep-01, Volume: 123 A wealth of evidence has shown that opioid and kinin systems may control proximal defense in the dorsal periaqueductal gray matter (dPAG), a critical panic-associated area. Studies with drugs that interfere with serotonin-mediated neurotransmission suggest that the μ-opioid receptor (MOR) synergistically interacts with the 5-HT Topics: Analgesics, Opioid; Angiotensin-Converting Enzyme Inhibitors; Animals; Anti-Anxiety Agents; Bradykinin; Bradykinin B2 Receptor Antagonists; Captopril; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Escape Reaction; Male; Panic; Periaqueductal Gray; Rats, Wistar; Receptor, Bradykinin B2; Receptors, Opioid, mu; Somatostatin	2017
Activity of tachykinin NK1 and bradykinin B2 receptor antagonists, and an opioid ligand at different stimulation parameters in neurogenic inflammation in the rat. Neuroscience letters, 1998, Nov-20, Volume: 257, Issue:1 Stimulation of the saphenous nerve in the anaesthetised rat results in cutaneous neurogenic oedema formation. We have examined the effect of a tachykinin NK1 and a bradykinin B2 antagonist, and a mu-opioid agonist on plasma extravasation observed in response to two differing nerve stimulating parameters (10 V, 1 ms, 2 Hz and 25 V, 2 ms, 10 Hz). The NK1 antagonist SR140333 abolished oedema, supporting the theory that an NK1 agonist is a primary mediator of neurogenic oedema. The B2 antagonist HOE 140 had no effect, indicating a lack of involvement of B2 receptors in this response. The pre-junctionally acting mu-opioid agonist DAMGO significantly inhibited oedema formation at the 10 V, 1 ms, 2 Hz (P < 0.001), but not the 25 V, 2 ms, 10 Hz stimulation parameters. Thus a post-junctionally acting NK1 antagonist inhibited neurogenic oedema formation induced by both stimulation parameters, whilst a pre-junctionally acting mu-opioid agonist acted only at 10 V, 1 ms, 2 Hz parameters. These findings could be of interest with respect to therapeutic approaches of pathophysiological conditions which involve a neurogenic component. Topics: Animals; Bradykinin; Bradykinin Receptor Antagonists; Edema; Electric Stimulation; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Enkephalins; Extravasation of Diagnostic and Therapeutic Materials; Male; Neurogenic Inflammation; Neurokinin-1 Receptor Antagonists; Neurons, Afferent; Peptide Fragments; Piperidines; Quinuclidines; Rats; Rats, Wistar; Receptor, Bradykinin B2; Receptors, Neurokinin-1; Receptors, Opioid, mu; Substance P; Time Factors	1998

Article

Year

Panicolytic-like action of bradykinin in the dorsal periaqueductal gray through μ-opioid and B2-kinin receptors.

Neuropharmacology, 2017, Sep-01, Volume: 123

A wealth of evidence has shown that opioid and kinin systems may control proximal defense in the dorsal periaqueductal gray matter (dPAG), a critical panic-associated area. Studies with drugs that interfere with serotonin-mediated neurotransmission suggest that the μ-opioid receptor (MOR) synergistically interacts with the 5-HT

Topics: Analgesics, Opioid; Angiotensin-Converting Enzyme Inhibitors; Animals; Anti-Anxiety Agents; Bradykinin; Bradykinin B2 Receptor Antagonists; Captopril; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Escape Reaction; Male; Panic; Periaqueductal Gray; Rats, Wistar; Receptor, Bradykinin B2; Receptors, Opioid, mu; Somatostatin

2017

Activity of tachykinin NK1 and bradykinin B2 receptor antagonists, and an opioid ligand at different stimulation parameters in neurogenic inflammation in the rat.

Neuroscience letters, 1998, Nov-20, Volume: 257, Issue:1

Stimulation of the saphenous nerve in the anaesthetised rat results in cutaneous neurogenic oedema formation. We have examined the effect of a tachykinin NK1 and a bradykinin B2 antagonist, and a mu-opioid agonist on plasma extravasation observed in response to two differing nerve stimulating parameters (10 V, 1 ms, 2 Hz and 25 V, 2 ms, 10 Hz). The NK1 antagonist SR140333 abolished oedema, supporting the theory that an NK1 agonist is a primary mediator of neurogenic oedema. The B2 antagonist HOE 140 had no effect, indicating a lack of involvement of B2 receptors in this response. The pre-junctionally acting mu-opioid agonist DAMGO significantly inhibited oedema formation at the 10 V, 1 ms, 2 Hz (P < 0.001), but not the 25 V, 2 ms, 10 Hz stimulation parameters. Thus a post-junctionally acting NK1 antagonist inhibited neurogenic oedema formation induced by both stimulation parameters, whilst a pre-junctionally acting mu-opioid agonist acted only at 10 V, 1 ms, 2 Hz parameters. These findings could be of interest with respect to therapeutic approaches of pathophysiological conditions which involve a neurogenic component.

Topics: Animals; Bradykinin; Bradykinin Receptor Antagonists; Edema; Electric Stimulation; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Enkephalins; Extravasation of Diagnostic and Therapeutic Materials; Male; Neurogenic Inflammation; Neurokinin-1 Receptor Antagonists; Neurons, Afferent; Peptide Fragments; Piperidines; Quinuclidines; Rats; Rats, Wistar; Receptor, Bradykinin B2; Receptors, Neurokinin-1; Receptors, Opioid, mu; Substance P; Time Factors

1998