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Regional anaesthesia
Published in Daryl Dob, Griselda Cooper, Anita Holdcroft, Philip Steer, Gwyneth Lewis, Crises in Childbirth Why Mothers Survive, 2018
Michael Kinsella, Daryl Dob, Anita Holdcroft
For many years ephedrine was the only acceptable drug for prophylaxis and treatment of hypotension after obstetric regional anaesthesia. This situation was based on its superiority in preserving uterine blood flow in a sheep model, compared with α-adrenergic agonists during intravenous infusion.45 However, extensive clinical research has demonstrated that ephedrine is associated with greater neonatal acidosis than are α-adrenergic agonists, probably mediated through direct placental transfer leading to altered fetal metabolism.46 This effect is dose dependent.47 Ephedrine as an indirect agonist leads to catecholamine release that stimulates both α- and β-adrenergic receptors, resulting in increased cardiac output in addition to vasoconstriction. However, as a result, tachyphylaxis may occur. Large prophylactic doses may also result in frequent hypertension.47
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
An agonist is a DRUG or chemical that is able to bind to a RECEPTOR and activate it, producing an appropriate response which may involve changes in ION CHANNEL opening or closing, activation of SECOND MESSENGERS and changes in neuronal FIRING. An agonist effectively mimics whatever effect the natural LIGAND for a receptor has. Such agonists are called DIRECT AGONISTS. It is important to note that receptors may have multiple binding sites present on them: the principal site is that at which the neurotransmitter binds, but there may be other sites at which neuromodulators or co-transmitters bind (see NEUROMODULATION). An INDIRECT AGONIST is one which binds to a site on receptor other than the main biding site for the ligand. In doing so it interferes with the action of the receptor, facilitating actions there. An INVERSE
Palmitoylethanolamide: A Potential Alternative to Cannabidiol
Published in Journal of Dietary Supplements, 2023
Paul Clayton, Silma Subah, Ruchitha Venkatesh, Mariko Hill, Nathasha Bogoda
Apart from ECS regulation, CBD’s mechanistic pathways include activation of non-cannabinoid receptors such as non-GPCR PPAR- γ and ligand-gated ion channels TRPV1 (72, 73). It is also reported to interact with opioid, serotonin, adenosine and GABA receptors (72). Interactions through TRPV1, opioid-sparing effect and regulating the EC tones have been associated with CBD’s anti-inflammatory, analgesic and temperature modulating effect (73, 74). Direct and/or indirect agonist action at HT1A receptors is considered to account for CBD’s anxiolytic and antiemetic effects (75, 76).