scholarly journals Studying Nitric Oxide in the Developing Retina: Neuromodulatory Functions and Signaling Mechanisms

2013 ◽  
Vol 5 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Renato Socodato
Keyword(s):  
Nitric Oxide ◽  
Signaling Mechanisms

Mechanisms of calcium signaling by cyclic ADP-ribose and NAADP

1997 ◽  
Vol 77 (4) ◽  
pp. 1133-1164 ◽  
Author(s):  
H. C. Lee
Keyword(s):  
Nitric Oxide ◽  
Nicotinic Acid ◽  
Live Cells ◽  
Release Mechanism ◽  
Major Mechanism ◽  
Signaling Mechanisms ◽  
Signaling Function ◽  
Cyclic Adp Ribose ◽  
Inositol 1,4,5 Trisphosphate ◽  
External Signals

Cells possess various mechanisms for transducing external signals to intracellular responses. The discovery of inositol 1,4,5-trisphosphate (IP3) as a messenger for mobilizing internal Ca2+ stores has centralized Ca2+ mobilization among signaling mechanisms. Results reviewed in this article establish that, in addition to IP3, the internal Ca2+ stores can be mobilized by at least two other molecules, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), via totally independent mechanisms. Cyclic ADP-ribose is a newly discovered cyclic nucleotide derived from NAD, but, unlike adenosine 3',5'-cyclic monophosphate, its main signaling function is modulation of Ca(2+)-induced Ca2+ release, a major mechanism of Ca2+ mobilization in addition to the IP3 pathway. Evidence shows that cADPR may in fact be responsible for mediating the Ca(2+)-mobilizing activity of the gaseous messenger nitric oxide. Cells responsive to cADPR are widespread and include species from plant to mammal, indicating the generality of cADPR as a signaling molecule. In addition to cADPR, NAADP, a metabolite of NADP, can also mobilize Ca2+ stores. The release mechanism and the stores on which NAADP acts are distinct from cADPR and IP3. Nicotinic acid adenine dinucleotide phosphate may play a role in generating Ca2+ oscillations, since liberation of NAADP in live cells by photolyzing its caged analog produces long lasting Ca2+ oscillations. These two new Ca2+ agonists are intimately related, since the same metabolic enzymes can, under appropriate conditions, synthesize either one, suggesting a unified mechanism may regulate both pathways. Elucidation of these two new Ca2+ mobilization pathways is likely to have an important impact on our understanding of cellular signaling mechanisms.

scholarly journals Statin-Induced Nitric Oxide Signaling: Mechanisms and Therapeutic Implications

2019 ◽  
Vol 8 (12) ◽  
pp. 2051 ◽  
Author(s):  
Armita Mahdavi Gorabi ◽  
Nasim Kiaie ◽  
Saeideh Hajighasemi ◽  
Maciej Banach ◽  
Peter E. Penson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Blood Pressure ◽  
Atherosclerotic Plaques ◽  
Therapeutic Effects ◽  
Therapeutic Implications ◽  
Nitric Oxide Signaling ◽  
Beneficial Effects ◽  
Signaling Mechanisms ◽  
Neurological Injuries

In addition to their cholesterol-lowering effects, statins are associated with pleiotropic effects including improvements in heart failure (HF), reduced blood pressure, prevention of the rupture of atherosclerotic plaques and improved angiogenesis. In addition to these cardiovascular benefits, statins have been implicated in the treatment of neurological injuries, cancer, sepsis, and cirrhosis. These cholesterol-independent beneficial effects of statins are predominantly mediated through signaling pathways leading to increased production and bioavailability of nitric oxide (NO). In this review, the mechanistic pathways and therapeutic effects of statin-mediated elevations of NO are described and discussed.

scholarly journals Nitric Oxide Signaling in Plants

Plants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1550
Author(s):  
John T. Hancock
Keyword(s):  
Nitric Oxide ◽  
Cell Signaling ◽  
Developmental Stages ◽  
Physiological Responses ◽  
Post Translational Modifications ◽  
Nitric Oxide Signaling ◽  
Signaling Mechanisms ◽  
Oxide Synthase ◽  
Signaling Components ◽  
Aperture Closure

Nitric oxide (NO) is an integral part of cell signaling mechanisms in animals and plants. In plants, its enzymatic generation is still controversial. Evidence points to nitrate reductase being important, but the presence of a nitric oxide synthase-like enzyme is still contested. Regardless, NO has been shown to mediate many developmental stages in plants, and to be involved in a range of physiological responses, from stress management to stomatal aperture closure. Downstream from its generation are alterations of the actions of many cell signaling components, with post-translational modifications of proteins often being key. Here, a collection of papers embraces the differing aspects of NO metabolism in plants.

Flexible Couplings: Diffusing Neuromodulators and Adaptive Robotics

2005 ◽  
Vol 11 (1-2) ◽  
pp. 139-160 ◽  
Author(s):  
Andy Philippides ◽  
Phil Husbands ◽  
Tom Smith ◽  
Michael O'Shea
Keyword(s):  
Neural Network ◽  
Nitric Oxide ◽  
Artificial Neural Network ◽  
Nervous System ◽  
Evolutionary Robotics ◽  
Neurotransmitter Receptors ◽  
Loose Coupling ◽  
Receptor Model ◽  
Signaling Mechanisms ◽  
Artificial Neural Network Ann

Recent years have seen the discovery of freely diffusing gaseous neurotransmitters, such as nitric oxide (NO), in biological nervous systems. A type of artificial neural network (ANN) inspired by such gaseous signaling, the GasNet, has previously been shown to be more evolvable than traditional ANNs when used as an artificial nervous system in an evolutionary robotics setting, where evolvability means consistent speed to very good solutions—here, appropriate sensorimotor behavior-generating systems. We present two new versions of the GasNet, which take further inspiration from the properties of neuronal gaseous signaling. The plexus model is inspired by the extraordinary NO-producing cortical plexus structure of neural fibers and the properties of the diffusing NO signal it generates. The receptor model is inspired by the mediating action of neurotransmitter receptors. Both models are shown to significantly further improve evolvability. We describe a series of analyses suggesting that the reasons for the increase in evolvability are related to the flexible loose coupling of distinct signaling mechanisms, one “chemical” and one “electrical.”

scholarly journals Mechanisms Mediating Functional Hyperemia in the Brain

2017 ◽  
Vol 24 (1) ◽  
pp. 73-83 ◽  
Author(s):  
Amy R. Nippert ◽  
Kyle R. Biesecker ◽  
Eric A. Newman
Keyword(s):  
Nitric Oxide ◽  
Arachidonic Acid ◽  
Final Section ◽  
Neurovascular Coupling ◽  
Functional Hyperemia ◽  
Generating Functional ◽  
Signaling Mechanisms ◽  
The Brain ◽  
Astrocyte Endfeet

Neuronal activity within the brain evokes local increases in blood flow, a response termed functional hyperemia. This response ensures that active neurons receive sufficient oxygen and nutrients to maintain tissue function and health. In this review, we discuss the functions of functional hyperemia, the types of vessels that generate the response, and the signaling mechanisms that mediate neurovascular coupling, the communication between neurons and blood vessels. Neurovascular coupling signaling is mediated primarily by the vasoactive metabolites of arachidonic acid (AA), by nitric oxide, and by K+. While much is known about these pathways, many contentious issues remain. We highlight two controversies, the role of glial cell Ca2+ signaling in mediating neurovascular coupling and the importance of capillaries in generating functional hyperemia. We propose signaling pathways that resolve these controversies. In this scheme, capillary dilations are generated by Ca2+ increases in astrocyte endfeet, leading to production of AA metabolites. In contrast, arteriole dilations are generated by Ca2+ increases in neurons, resulting in production of nitric oxide and AA metabolites. Arachidonic acid from neurons also diffuses into astrocyte endfeet where it is converted into additional vasoactive metabolites. While this scheme resolves several discrepancies in the field, many unresolved challenges remain and are discussed in the final section of the review.

scholarly journals Mechanisms of ATP-mediated vasodilation in humans: modest role for nitric oxide and vasodilating prostaglandins

2011 ◽  
Vol 301 (4) ◽  
pp. H1302-H1310 ◽  
Author(s):  
Anne R. Crecelius ◽  
Brett S. Kirby ◽  
Jennifer C. Richards ◽  
Leora J. Garcia ◽  
Wyatt F. Voyles ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Steady State ◽  
Venous Occlusion ◽  
High Dose ◽  
Healthy Humans ◽  
Vasodilatory Response ◽  
Signaling Mechanisms ◽  
Before And After ◽  
Forearm Vascular Conductance ◽  
High Doses

ATP is an endothelium-dependent vasodilator, and findings regarding the underlying signaling mechanisms are equivocal. We sought to determine the independent and interactive roles of nitric oxide (NO) and vasodilating prostaglandins (PGs) in ATP-mediated vasodilation in young, healthy humans and determine whether any potential role was dependent on ATP dose or the timing of inhibition. In protocol 1 ( n = 18), a dose-response curve to intrabrachial infusion of ATP was performed before and after both single and combined inhibition of NO synthase [ NG-monomethyl-l-arginine (l-NMMA)] and cyclooxygenase (ketorolac). Forearm blood flow (FBF) was measured via venous occlusion plethysmography and forearm vascular conductance (FVC) was calculated. In this protocol, neither individual nor combined NO/PG inhibition had any effect on the vasodilatory response ( P = 0.22–0.99). In protocol 2 ( n = 16), we determined whether any possible contribution of both NO and PGs to ATP vasodilation was greater at low vs. high doses of ATP and whether inhibition during steady-state infusion of the respective dose of ATP impacted the dilation. FBF in this protocol was measured via Doppler ultrasound. In protocol 2, infusion of low ( n = 8)- and high-dose ( n = 8) ATP for 5 min evoked a significant increase in FVC above baseline (low = 198 ± 24%; high = 706 ± 79%). Infusion of l-NMMA and ketorolac together reduced steady-state FVC during both low- and high-dose ATP ( P < 0.05), and in a subsequent trial with continuous NO/PG blockade, the vasodilator response from baseline to 5 min of steady-state infusion was similarly reduced for both low (ΔFVC = −31 ± 11%)- and high-dose ATP (ΔFVC −25 ± 11%; P = 0.70 low vs. high dose). Collectively, our findings indicate a potential modest role for NO and PGs in the vasodilatory response to exogenous ATP in the human forearm that does not appear to be dose or timing dependent; however, this is dependent on the method for assessing forearm vascular responses. Importantly, the majority of ATP-mediated vasodilation is independent of these putative endothelium-dependent pathways in humans.

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