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Nutraceuticals for Hypertension Control
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
Balázs Varga, Mariann Bombicz, Andrea Kurucz, Béla Juhász
The major components of alliums, including onion, are organopolysulfides. The preventive potency of polysulfides in different chronic diseases including cancer, obesity, metabolic syndrome, gastric ulcer and cardiovascular disorders are well-known. The mechanism of polysulfides in cardioprotection are based on its hydrogen sulfide (H2S) donor property. H2S, next to nitric oxide (NO) and carbon monoxide (CO), is the third gasotransmitter and synthesized enzymatically from l-cysteine or l-homocysteine. H2S exerts its endotheliumdependent vasorelaxation by three main mechanisms: 1) activating NO synthase and inhibiting cGMP degradation by phosphodiesterase 5 (PDE5), thus potentiating the effect of NO-cGMP pathway; 2) H2S-derived polysulfides directly activate protein kinase G; and finally 3) H2S interacts with NO to form nitroxyl (HNO)-a potent vasorelaxant (Beltowski and Jamroz-Wisniewska 2014). Sakai et al. support this with their in vivo experiment on NO synthase inhibitor-induced hypertensive rats and spontaneously hypertensive rats (2003).
The Role of Fecal Microbiota Transplantation in Neurological Diseases
Published in David Perlmutter, The Microbiome and the Brain, 2019
Thomas Borody, John Bienenstock
The human gut archaea have been poorly studied and characterized in both healthy and diseased individuals. Unfortunately, our understanding of their potential role in influencing the MGBA is therefore limited. However, studies have shown that their abundance and distribution is distinctly affected by diet.25,26 Although evidence detailing the role of archaea in the MGBA is limited, it is undeniable that the human gastrointestinal tract contains a highly diverse population of archaea, specifically methanobacteriaceae,27 which exist as commensal and mutualistic organisms. These archaea synthesize methane in the gut, which is a gasotransmitter and has been shown to possess stimulatory effects on the enteric nervous system and ileal motor contractions.28
Heme Oxygenase-1 in Kidney Health and Disease
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Pu Duann, Elias A. Lianos, Pei-Hui Lin
Along with its catabolic products (biliverdin/bilirubin, CO, Fe2+), HO and its metabolites which often are induced in response to cellular injury and stress and play significant functions (reviewed in refs (28–30). CO is an autocrine and paracrine vasodilator in cerebral and systemic circulations (31,32) and functions as the second gasotransmitter in the GI tract (33,34). Bilirubin is a free radical scavenger and cellular antioxidant (35–37). Iron and the induced ferritin, a highly conserved iron-binding protein, is a key protein in protection from oxidative stress and the maintenance of cellular iron homeostasis (38,39).
Understanding hydrogen sulfide signaling in neonatal airway disease
Published in Expert Review of Respiratory Medicine, 2021
Marta Schiliro, Colleen M Bartman, Christina Pabelick
Gasotransmitters, terminology first coined in 2002 by Wang and colleagues [12], are small gaseous molecules that are endogenously and enzymatically produced in a regulated manner and freely diffuse through cellular membranes where they interact with and influence the function of a multitude of cellular targets [12,119]. The discovery of gasotransmitters changed the typical concept of intracellular signaling [6]. For example, gasotransmitters are not stored in vesicles but instead are produced on an as-needed basis, demonstrating the importance of enzymes involved in H2S metabolism to be under strict regulation. Another unique property of gasotransmitters is that they do not act with a classical secondary messenger cascade, but rather act through chemical modification of target proteins and subsequent immediate influence on cellular metabolism and other basic biological processes [6].
Spasmolytic activity of Aquilariae Lignum Resinatum extract on gastrointestinal motility involves muscarinic receptors, calcium channels and NO release
Published in Pharmaceutical Biology, 2018
Huimin Li, Yanfei Qu, Jiawei Zhang, Jingze Zhang, Wenyuan Gao
Furthermore, we explored if the antispasmodic activity displayed by ALR was mediated by gasotransmitters. Therefore, the effects of ALR on pretreatment with l-NAME (10−4 M, an inhibitor of nitric oxide synthase (NOS)) and PAG (10−5 M, an inhibitor of cystathionine-γ-lyase) of rat-isolated jejunum were tested. The results showed that relaxation curves of ALR were significantly displaced to the right pretreatment with l-NAME (p < 0.01), but not modified by PAG (p > 0.05). NO acts as a signalling molecule in vascular and GI smooth muscle. It is a vital gasotransmitter in numerous physiological and inflammatory processes (Moncada et al. 1991). Since a series of studies have demonstrated that NOS is present in the myenteric plexus, NO has become a most likely candidate for mediating nonadrenergic–noncholinergic smooth muscle relaxation through the GI tract (Ragy and Elbassuoni 2012). Endogenous NO from the smooth muscle is capable of regulating contractile tone. NO can activate soluble guanylyl cyclase (sGC) which increases the production of intracellular cyclic guanosine monophosphate (cGMP). The increase of cGMP results in the activation of protein kinase G that suppresses calcium influx and reduces the sensitivity of contractile elements to calcium (Ventura-Martínez et al. 2011). All these findings clearly revealed that the relaxation evoked by ALR was mediated by NOS–NO–cGMP signalling pathway.
Hydrogen sulfide: a target to modulate oxidative stress and neuroplasticity for the treatment of pathological anxiety
Published in Expert Review of Neurotherapeutics, 2020
Mary Chen, Caroline Pritchard, Diandra Fortune, Priyadurga Kodi, Marco Grados
H2S is a gasotransmitter, alongside the signaling molecules nitrous oxide (NO) and carbon monoxide (CO). As a potentially toxic agent, H2S levels are tightly regulated via cross-talk between NO and CO pathways, both of which can influence the heme moiety of CBS and regulate H2S production [23]. In the liver, S-sulfhydration activates up to one-quarter of proteins, including actin, tubulin, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) [24]. In the CNS, H2S is present at a concentration of approximately 50–160 μmol [25]. Meanwhile, recent data suggest that the concentration in blood is low micromolar only [26], although it is plausibly higher in the CNS.