Diffusion of Nitric Oxide in the Aorta Wall Monitored in Situ by Porphyrinic Microsensors

Malinski, T.; Taha, Ziad; Grunfeld, Saul; Patton, Stephen R.; Kapturczak, Matthias H.; Tomboulian, Paul

doi:10.1006/bbrc.1993.1735

Cited by 399 publications

(254 citation statements)

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“…Studies designed to measure the distance of NO Å diffusion under physiological conditions by means of electrochemical microsensors reported values of 100-200 lm, rising within 10-15 s to a steady-state concentration, which are consistent with a high diffusion coefficient, 3300 lm 2 /s (Malinski et al, 1993;Meulemans, 1994). A first strong experimental evidence for the intercellular diffusion of NO Å in the brain came from the work of Schuman and Madison that were able to show NO Å -induced synaptic potentiation between paired neurons and synapses approximately 100 lm distant in hippocampal slices (Schuman and Madison, 1994).…”

Section: Diffusion and Regulation Of Nitric Oxide Activity In The Brainmentioning

confidence: 69%

Nitric oxide in brain: diffusion, targets and concentration dynamics in hippocampal subregions

Ledo

Frade

Barbosa

et al. 2004

Molecular Aspects of Medicine

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Nitric oxide (NO Å ) is a diffusible regulatory molecule involved in a wide range of physiological and pathological events. At the tissue level, a local and temporary increase in NO Å concentration is translated into a cellular signal. From our current knowledge of biological synthesis and decay, the kinetics and mechanisms that determine NO Å concentration dynamics in tissues are poorly understood. Generally, NO Å mediates its effects by stimulating (e.g., guanylate cyclase) or inhibiting (e.g., cytochrome oxidase) transition metal-containing proteins and by post-translational modification of proteins (e.g., formation of nitrosothiol adducts). The borderline between the physiological and pathological activities of NO Å is a matter of controversy, but tissue redox environment, supramolecular organization and compartmentalisation of NO Å targets are important features in determining NO Å actions. In brain, NO Å synthesis in the dependency of glutamate NMDA receptor is a paradigmatic example; the NMDA-subtype glutamate receptor triggers intracellular signalling pathways that govern neuronal plasticity, development, senescence and disease, suggesting a role for NO Å in these processes. Measurements of NO Å in the different subregions of hippocampus, in a glutamate NMDA receptor-dependent fashion, by means of electrochemical selective microsensors illustrate the concentration dynamics of NO Å in the sub-regions of this brain area. The analysis of NO Å concentration-time profiles in the hippocampus requires consideration of at least two interrelated issues, also addressed in this review. NO Å diffusion in a biological medium and regulation of NO Å activity. Ó 2004 Elsevier Ltd. All rights reserved.Abbreviations: CAPON, Carboxy-terminal PDZ ligand of nNOS; DOPAC, dihydroxyphenylacetic acid; EPR, electron paramagnetic resonance; LTP, long-term potentiation; NMDA, N-methyl-D D -aspartate; NOS, nitric oxide synthase; PDZ, PSD-95 discs large/ZO-1 homology domain; PSD-95, post-synaptic density protein 95

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Section: Diffusion and Regulation Of Nitric Oxide Activity In The Brainmentioning

confidence: 69%

Nitric oxide in brain: diffusion, targets and concentration dynamics in hippocampal subregions

Ledo

Frade

Barbosa

et al. 2004

Molecular Aspects of Medicine

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“…By increasing the concentration of NO, once saturation of SO has occurred, the excess NO is available to act in the endoderm. Furthermore, NO is membrane permeable, unlike SO, and capable of diffusing over 100 µm in a few seconds at 37°C (Meulemans, 1994;Wise and Houghton, 1969;Malinski et al, 1993a;Malinski et al, 1993b). NO has been demonstrated to diffuse through tissues without consumption, establishing its role as an intracellular messenger (Lancaster, 1994;Wood and Garthwaite, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…As eNOS produces a lower concentration of NO than does the iNOS isoform, we expect the physiological concentration of NO during normal development in the endothelium to be low. In other tissues, such as the cerebrum, the concentration of NO was measured at 10 nM during physiological conditions (Malinski et al, 1993a;Malinski et al, 1993b). Furthermore, only 5 nM of NO is needed to induce relaxation of vessels and is the minimum concentration to activate guanylate cyclase.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

et al. 2004

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Nitric oxide (NO) has been demonstrated to mediate events during ovulation,pregnancy, blastocyst invasion and preimplantation embryogenesis. However,less is known about the role of NO during postimplantation development. Therefore, in this study, we explored the effects of NO during vascular development of the murine yolk sac, which begins shortly after implantation. Establishment of the vitelline circulation is crucial for normal embryonic growth and development. Moreover, functional inactivation of the endodermal layer of the yolk sac by environmental insults or genetic manipulations during this period leads to embryonic defects/lethality, as this structure is vital for transport, metabolism and induction of vascular development. In this study, we describe the temporally/spatially regulated distribution of nitric oxide synthase (NOS) isoforms during the three stages of yolk sac vascular development (blood island formation, primary capillary plexus formation and vessel maturation/remodeling) and found NOS expression patterns were diametrically opposed. To pharmacologically manipulate vascular development,an established in vitro system of whole murine embryo culture was employed. During blood island formation, the endoderm produced NO and inhibition of NO(L-NMMA) at this stage resulted in developmental arrest at the primary plexus stage and vasculopathy. Furthermore, administration of a NO donor did not cause abnormal vascular development; however, exogenous NO correlated with increased eNOS and decreased iNOS protein levels. Additionally, a known environmental insult (high glucose) that produces reactive oxygen species(ROS) and induces vasculopathy also altered eNOS/iNOS distribution and induced NO production during yolk sac vascular development. However, administration of a NO donor rescued the high glucose induced vasculopathy, restored the eNOS/iNOS distribution and decreased ROS production. These data suggest that NO acts as an endoderm-derived factor that modulates normal yolk sac vascular development, and decreased NO bioavailability and NO-mediated sequela may underlie high glucose induced vasculopathy.

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“…Here D is the diffusion coefficient of NO in tissue, which has been measured experimentally as 3300 µm 2 s −1 (Malinski et al, 1993). We have solved these equations numerically in the two-dimensional (2D) spatial domain illustrated in Fig.…”

Section: Mathematical Modelmentioning

confidence: 99%

Modelling Blood Flow Regulation by Nitric Oxide in Psoriatic Plaques

Sherratt

Weller

Savill

2002

Bulletin of Mathematical Biology

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Psoriasis is a common skin disease, with a clinical appearance of red, scaly lesions, known as plaques. Recent experimental research has shown that the ubiquitous cellsignalling molecule nitric oxide (NO) is actively synthesized within these plaques by the iNOS enzyme. In contrast, NO production from normal, healthy skin is a byproduct of the reduction of nitrite in sweat. Measurement of NO release rates at the skin surface are 100 times greater from psoriatic lesions than normal skin. We propose a mathematical model for the dynamics of NO within psoriatic plaques, that incorporates diffusion, production in the basal epidermis, decay within the plaque, and active scavenging by red blood cell haemoglobin; this last effect introduces a key nonlinearity into the model. We present numerical simulations of the model in two space dimensions, and then describe an approximation that reduces the model to two coupled ordinary differential equations. This reduced system can be solved exactly, giving an approximation for the NO release rate as an explicit function of model parameters. We use this approximation to explain some recent, surprising experimental results.

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Diffusion of Nitric Oxide in the Aorta Wall Monitored in Situ by Porphyrinic Microsensors

Cited by 399 publications

References 0 publications

Nitric oxide in brain: diffusion, targets and concentration dynamics in hippocampal subregions

Nitric oxide in brain: diffusion, targets and concentration dynamics in hippocampal subregions

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

Modelling Blood Flow Regulation by Nitric Oxide in Psoriatic Plaques

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