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Local Regulation of Endothelium-Dependent Responses
Published in Thomas F. Lüscher, Paul M. Vanhoutte, The Endothelium: Modulator of Cardiovascular Function, 2020
Thomas F. Lüscher, Paul M. Vanhoutte
Endothelial cells can form histamine (see Chapter 5). The vascular response to histamine depends on the number and distribution of inhibitory and excitatory receptors located on endothelial cells, vascular smooth muscle, and autonomic nerve endings (Figure 9)117,402,403,412,677,1126,1261,1262,1294,1340,1423 In a variety of isolated arteries, including human arteries, histamine causes endothelium-dependent relaxations. The available evidence strongly suggests that in most blood vessels Hi- rather than H2-histaminergic receptors mediate the endothelium-dependent relaxations evoked by histamine (Figure 10).3,493,621,771,1262,1294,1423 Bioassay experiments with human umbilical vessels (both arteries and veins) and cultured human umbilical endothelial cells demonstrate the ability of histamine to release EDRF.1297 It is unknown whether or not endothelium-derived histamine activates histaminergic receptors on neighboring cells.
Sleep and Dermatology
Published in S.R. Pandi-Perumal, Meera Narasimhan, Milton Kramer, Sleep and Psychosomatic Medicine, 2017
A. Gupta Madhulika, K. Gupta Aditya, Knapp Katie
Urticaria or hives are characterized by transient skin or mucosal swelling, resulting in wheals due to plasma leakage.119 Urticaria is defined as chronic after a period of time of usually ≥6 weeks. The lifetime occurrence of urticaria ranges from <1% to 30%.119 In over 50% of cases, the basis for the urticaria is not found. The mast cell is the primary effector cell of urticaria. Mast cell granules contain preformed mediators of inflammation, the most important of which is histamine.119 Histamine is a major wake-promoting neurotransmitter in the CNS, and histaminergic neurons display elevated discharge activity during increased states of vigilance.120
Stimulus-Secretion Coupling: Receptors
Published in Stephen W. Carmichael, Susan L. Stoddard, The Adrenal Medulla 1986 - 1988, 2017
Stephen W. Carmichael, Susan L. Stoddard
Noble, Bommer, Liebisch et al. (1988) reported that histamine as well as other neuroactive substances stimulated the release of catecholamines from bovine adrenal chromaffin cells. Histamine stimulation was found to be dose-dependent and occurred through activation of histaminergic receptors. In contrast to cholinergic nicotinic activation, histamine initially induced a small release of catecholamines but, with prolonged exposure, it produced a much greater response than nicotine did. In addition, the H1-receptor showed little desensitization over time. This histamine-induced release was found to be calcium-dependent and was attenuated by calcium channel blockers. These studies suggest that histamine as well as certain other neuroactive substances could play an important role in the physiology and biochemistry of adrenal chromaffin cells.
Switching to long-acting injectable antipsychotics: pharmacological considerations and practical approaches
Published in Expert Opinion on Pharmacotherapy, 2023
Mikkel Højlund, Christoph U. Correll
Histaminergic and cholinergic rebound occurs when switching from antipsychotics with potent antihistaminergic or anticholinergic properties (e.g. clozapine, olanzapine, or quetiapine) to antipsychotics with lower affinity to these receptors (e.g. risperidone or aripiprazole). The histaminergic and cholinergic blockade will calm anxiety and agitation, improve sleep, and possibly also counter extrapyramidal symptoms (EPS) resulting from dopaminergic blockade. Conversely, these properties also mean that abrupt discontinuation can result in the opposite symptoms (e.g. rebound anxiety, agitation, insomnia, akathisia) because an increased number of histaminergic or cholinergic receptors that may also be in a high-affinity state suddenly are left free to stimulation by endogenous histamine and acetylcholine.
Hypolipemic effects of histamine is due to inhibition of VLDL secretion from the liver: involvement of both H1 and H2-receptors
Published in Archives of Physiology and Biochemistry, 2022
Stimulation of lipolysis in adipose tissue is another way whereby histamine affects plasma lipids in vivo. In vivo experiments indicated that histamine stimulates lipolysis in fat tissue through H2-receptors and increases free fatty acids (Akiyama et al.1990). A similar result has been shown in the cultures of canine fat cells (Bugajski and Gadek 1985). A central histaminergic pathway also may be involved. It is well indicated that plasma free fatty acids stimulates directly the rate of VLDL secretion from the liver (Rasouli et al.2016). Lipolysis in adipocytes is mediated through the cAMP pathway, which is also used in the H2-histaminergic signal transduction pathway. Thus, histamine has two opposite effects on the plasma lipids in vivo. Stimulation of lipolysis is mediated by the cAMP pathway (i.e. H2-receptors) at fat tissue and subsequently increases VLDL secretion from the liver. While stimulation of either Ca2+/calmodulin (H1-receptors) or cAMP (i.e. H2-receptors) inhibits VLDL secretion directly in the liver (Rasouli et al.2016, Wang et al.2010). Imoto et al. also have reported that histamine H1 receptors are more predominant than H2-histamine, adrenergic, and prostaglandin receptors on the liver plasma membrane (Imoto et al.1985).
The role of itch and pain modulation in the prediction of phototherapy outcomes: a prospective cohort study
Published in Journal of Dermatological Treatment, 2022
Michal Ramon, Sarit Yakov, Pora Kuperman, Michal Granot
Regarding the ascending sensory pathways, it has been proposed that hyperknesis, as well as alloknesis, were observed after electrically-evoked itch and itch provocations by histamine (27). The former is believed to perceptually represent centrally-mediated sensitization to input from A delta- or C- nociceptors enabling increased itch following pricking and itching mechanical stimuli. Indeed, non-histaminergic neuronal sensitization characterizes itch severity in atopic dermatitis patients who had enhanced mechanical pain sensitivity (28). These findings support the notion of mutual mechanisms of sensitization involved in pain and itch, although we found no significant role for enhanced pain facilitation. This may suggest that the inhibitory pathways play a more dominant role in the modulation of itch, though it may be also possible that the chosen paradigm to assess sensitization in our study was less sensitive and thus unable to reveal the contribution of ascending pathways.