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Perspective
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
So named because of the fast onset of their action, as opposed to the slower-acting bradykinin, tachykinins, also known as neurokinins, are a family of neuropep-tides with structural and biological features in common. Mammalian tachykinins comprise substance P and neurokinin A, derived from a single gene, and neurokinin B, derived from another. Tachykinins continue to be the focus of active investigation as to their distribution, localization in sensory nerves, co-localization with other neuropeptides such as calcitonin gene-related peptide (CGRP), biosynthesis, mode of action, specific receptors and receptor antagonists, degradation, and possible role in bronchial asthma and other inflammatory states (Chapters 4, 5, 6, 22).
Pain Sensitization
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
A number of peptides released by primary afferents have a role in nociception, and these include substance P, neurokinin A and CGRP. Substance P and neurokinin A act on neurokinin receptors. Other receptors such as opioid (μ, κ and δ), α-adrenergic, GABA, serotonin (5-HT) and adenosine receptors are also involved in nociceptive transmission or modulation. New drugs that act at the nicotinic acetylcholine receptor appear to provide strong analgesia without the withdrawal symptoms associated with opioids.
Renal, Cardiovascular, and Pulmonary Functions of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The control of the bronchial diameter is complex and involves both neural and humoral factors. Thus, adrenergic and cholinergic systems are both involved in this regulation, as well as inhibitory and excitatory non-adrenergic, non-cholinergic nerves. Adrenergic control is carried out by NE released from nerve endings and Epi released from the adrenal medulla. Acting via β2-AR, Epi and NE can produce bronchodilation, but they can also produce bronchoconstriction by stimulating α1 and α2 AR if pathological disturbances exist in the airways. Non-adrenergic/non-cholinergic nervous control of airway smooth muscle is exerted by neurotransmitters such as substance P, neurokinin, and neuropeptide Y.
Blocking SP/NK1R signaling improves spinal cord hemisection by inhibiting the release of pro-inflammatory cytokines in rabbits
Published in The Journal of Spinal Cord Medicine, 2023
Yuehuan Zheng, Nannan Wang, Zhe Chen, Liqiang Shi, Xiangyang Xu
The blood-spinal cord barrier is destroyed immediately after SCI, and the vascular permeability increases continuously for 7–8 weeks after the injury,5 allowing high-moleculary-weight inflammatory mediators to enter the central nervous system to exert neurotoxicity and impair neuronal function.6 Tachykinin is involved in the regulation of sensory and emotional responses and various neuronal signaling pathways.7 Substance P (SP), neurokinin A and neurokinin B are the three main tachykinins in mammals.7 Studies have shown that SP, a precursor neuropeptide, plays an important role in nociceptive activity at the spinal cord level in response to peripheral inflammation and nociceptive stimuli.8 In addition, SP can also induce increased microvascular permeability, vasodilatation and tissue edema, and is considered to be a key mediator of neurogenic inflammation.9 SP preferentially activates neurokinin 1 receptor (NK1R).10 The inhibitory effect of NK-1R antagonist on inflammatory response has been confirmed in spinal neuron,11 microglia12 and macrophages.13 Therefore, the SP-NK1R axis played an important role in the regulation of inflammation.
Identifying molecular mechanisms of acute to chronic pain transition and potential drug targets
Published in Expert Opinion on Therapeutic Targets, 2022
Kannan Aravagiri, Adam Ali, Hank C Wang, Kenneth D Candido, Nebojsa Nick Knezevic
Besides peripheral and central sensitization/priming, the dysregulation of inhibitory interneurons and descending neurons in the spinal cord and brain, specifically in the periaqueductal gray, rostral ventromedial medulla (RVM), and reticular formation, has also been known to be another contributing factor in the transition from acute to chronic pain. An example of dysregulated descending control that has been identified involves the RVM. In models of nerve and mechanical injury, it was found that activation of the RVM with the delivery of substance P to Neurokinin-1 (NK1) reduces inhibitory descending function and therefore maintains the pain state [24,25]. Another process in which this is done is through the production of dynorphin, an endogenous opioid that interacts with NMDA receptors to produce a prolonged pain-state [26]. Initially intended to activate opioid receptors and reduce pain in the short term, ongoing dynorphin release can cause opioid tolerance and therefore opioid-induced hyperalgesia (OIH). Another example of dysregulated descending control that has been identified involves the locus coeruleus (LCL). Activation of the LCL with noxious stimuli prompts the delivery of noradrenergic neurotransmitters and activation of α-2 receptors, allowing for the reduced release of activating neurotransmitters [27]. Both these areas become dysregulated and are implicated when discussing the transition from acute to chronic pain.
Managing vasomotor symptoms effectively without hormones
Published in Climacteric, 2020
C. A. McCormick, A. Brennan, M. Hickey
Menopause is a normal reproductive stage marking the end of reproductive life. Characteristic changes in ovarian sex steroid production lead to changes in menstrual bleeding patterns and commonly induce symptoms that may affect quality of life, work attendance and productivity, and intimate relationships1. Vasomotor symptoms (VMS; hot flushes and/or night sweats) affect around 80% of women over the menopause transition, are the main reason for seeking medical advice, and are the leading patient priority for treatment2. Currently, VMS are thought to result from upregulation of neurokinin B secondary to estrogen deficiency3. Neurokinin B interacts with the autonomic thermoregulatory pathway. Directly targeting this pathway is an area of growing clinical interest in non-hormonal treatments for VMS4.