Direct electrochemical measurement of nitric oxide in vascular endothelium

Brovkovych, Viktor; Stolarczyk, Elzbieta I.; Oman, Jason; Tomboulian, Paul; Maliński, Tadeusz

doi:10.1016/s0731-7085(98)00090-9

Cited by 86 publications

(61 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The hyperpolarization induced by this agonist was lower in the SHR than in the NWR vessels, indicating that NO release was deficient in the hypertensive animals. This agrees with previous findings in SHR mesenteric arteries 14 and in cultured endothelial cells, which show NO deficiency in SHR 21 caused by increased destruction by super oxide. 22,23 We followed the changes of carotid smooth muscle membrane potential as well as endothelin plasma concentration for several days after angioplasty (Figures 3 and 4).…”

Section: Discussionsupporting

confidence: 93%

Role of Membrane Potential and Expression of Endothelial Factors in Restenosis After Angioplasty in SHR

et al. 2004

View full text Add to dashboard Cite

Abstract-We examined the roles played by impaired K ϩ channels, diminished nitric oxide (NO) production, endothelin release, and smooth muscle membrane potential in the increased restenosis observed in spontaneously hypertensive rat (SHR) carotid arteries after angioplasty. The SHR carotid was found to be less polarized than that of normotensive Wistar rats (NWR), and it was further depolarized by the ␣ 2 agonist UK 14,304. This response was blocked by iberiotoxin, indicating that calcium-dependent K ϩ channels operate normally in the SHR carotid. Acetylcholine caused a hyperpolarization that was significantly smaller in SHR than in NWR carotids, indicating a deficient release of NO in the SHR. After angioplasty, SHR and NWR vessels were depolarized, returning to baseline after 10 days. In the SHR but not in the NWR the contralateral carotid was also depolarized, and this was prevented by the endothelin A/B receptor antagonist bosentan. After angioplasty, endothelin-1 plasma levels increased in both SHR and NWR, but the increase was significantly more prolonged in SHR. We found that the more pronounced restenosis observed in the SHR carotid after angioplasty is not due to impairment of calcium-dependent K ϩ channels but is related to the relatively depolarized vascular smooth muscles, involving endothelin release caused by reduced NO levels in that strain. Key Words: rats, spontaneously hypertensive Ⅲ angioplasty Ⅲ carotid arteries Ⅲ muscle smooth, vascular Ⅲ membranes Ⅲ endothelin T he vascular endothelium plays a role in blood flow control through the release of relaxant and contractile factors. Thus, to prevent overactivation of contractile responses, it releases relaxant factors such as endotheliumderived hyperpolarizing factor, prostanoids, and nitric oxide (NO). The endothelium also prevents the development of vascular lesions by inhibiting platelet aggregation, leukocyte adhesion, and proliferation of vascular smooth muscle cells. 1 This protective role is altered in pathological conditions such as arterial hypertension, which is characterized by cell permeability changes, leukocyte adhesion, and smooth muscle cell proliferation. Also, the repair mechanism designed to restore the vessel wall after damage from different causes frequently escapes self-limiting control, resulting in lumen narrowing caused by smooth muscle cell proliferation. These processes are the precursors of atherosclerotic plaque formation, which leads to increased vascular resistance and to restenosis. 2 Procedures such as atherectomy performed by balloon injury (angioplasty) widen the lumen but cause extensive endothelium destruction, leaving the vascular wall without protection. This injury stimulates medial smooth muscle cell proliferation and migration to the deendothelized surface to form a neointima. Neointima proliferation and subsequent vascular restenosis are believed to be the main events in the initiation of the atherosclerosis that limits the long-term efficacy of percutaneous transluminal coronary angioplasty. 3 It is well...

show abstract

Section: Discussionsupporting

confidence: 93%

Role of Membrane Potential and Expression of Endothelial Factors in Restenosis After Angioplasty in SHR

et al. 2004

View full text Add to dashboard Cite

show abstract

“…NO release was measured electrochemically in real time using nafion-coated porphyrinic microsensor, calibrated with standard NO solutions (17). In some experiments, platelets were preincubated with 200 M puromycin or vehicle control for 10 min.…”

Section: Methodsmentioning

confidence: 99%

Signaling-mediated Functional Activation of Inducible Nitric-oxide Synthase and Its Role in Stimulating Platelet Activation

Marjanovic¹,

Stojanović²,

Brovkovych

et al. 2008

Journal of Biological Chemistry

View full text Add to dashboard Cite

Nitric oxide (NO) is a short lived secondary messenger, synthesized by nitric-oxide synthases (NOS). It is believed that the activity of inducible NOS (iNOS) is regulated primarily at the transcription level by inducing expression of iNOS mRNA and protein, which then continuously produces NO, until its degradation. Platelets do not have the nuclear transcriptional regulatory mechanisms of the iNOS gene and are believed to generate NO in response to agonist stimulation via endothelial NOS (eNOS). However, here we show that agonist-induced NO production is only partially eNOS-dependent and is also mediated by iNOS. Platelet agonist-induced NO production is significantly reduced in iNOS-knockout platelets. Platelet NO production occurs within seconds after agonist addition and is not accompanied by changes in iNOS protein levels, indicating a signaling-mediated functional activation mechanism of iNOS. Importantly, iNOS knock-out and iNOS inhibitors reduce agonist-induced platelet secretion and aggregation and cGMP levels, indicating that iNOS activation is important in stimulating platelets via the newly identified NO-cGMP-dependent platelet secretion pathway. Furthermore, iNOS knock-out mice have prolonged bleeding time, suggesting that this novel mode of regulation of iNOS activity plays a physiologically relevant role in hemostasis.

show abstract

“…Electrochemical techniques have been applied to detect various reactive oxygen and nitrogen species [49][50][51][52][53][54]. Some of these utilize direct detection of diverse reactive species based on their differential redox potentials, while others use electrodes modified with molecules or proteins with electrocatalytic activity towards the species of interest.…”

Section: Electrochemistrymentioning

confidence: 99%

Redox regulation of calcium ion channels: Chemical and physiological aspects

et al. 2011

View full text Add to dashboard Cite

a b s t r a c tReactive oxygen species (ROS) are increasingly recognized as second messengers in many cellular processes. While high concentrations of oxidants damage proteins, lipids and DNA, ultimately resulting in cell death, selective and reversible oxidation of key residues in proteins is a physiological mechanism that can transiently alter their activity and function. Defects in ROS producing enzymes cause disturbed immune response and disease.Changes in the intracellular free Ca 2+ concentration are key triggers for diverse cellular functions. Ca 2+ homeostasis thus needs to be precisely tuned by channels, pumps, transporters and cellular buffering systems. Alterations of these key regulatory proteins by reversible or irreversible oxidation alter the physiological outcome following cell stimulation. It is therefore necessary to understand which proteins are regulated and if this regulation is relevant in a physiological-and/or pathophysiological context. Because ROS are inherently difficult to identify and to measure, we first review basic oxygen redox chemistry and methods of ROS detection with special emphasis on electron paramagnetic resonance (EPR) spectroscopy. We then focus on the present knowledge of redox regulation of Ca 2+ permeable ion channels such as voltage-gated (CaV) Ca 2+ channels, transient receptor potential (TRP) channels and Orai channels.© 2011 Elsevier Ltd. All rights reserved. Basic redox chemistry of oxygenMany chemical processes are linked to the exchange of electrons between two or more molecular entities. The transfer of one (or more) electron(s) is associated with oxidation (loss of electron) and reduction (gain of electron) of the components. Such reactions are also known as redox reactions. The processes of reactive oxygen species (ROS) formation and elimination are exclusively of redox nature.Molecular oxygen is the precursor of all ROS. It contains two unpaired electrons in separate (antibonding) orbitals in its outer electron sphere and is thus, by definition, a radical. Radicals have at least one unpaired electron in their orbital system and usually show high reactivity; transition metal ions also may have unpaired electrons, but are not called radicals. Although having radical character, molecular oxygen is chemically rather inert (luckily!), because high * Corresponding authors at: Institut für Biophysik, Gebäude 58, Universität des Saarlandes, D-66421 Homburg/Saar, Germany. Tel.: +49 6841 1626453; fax: +49 6841 1626060.E-mail addresses: ivan.bogeski@uks.eu (I. Bogeski), barbara.niemeyer@uks.eu (B.A. Niemeyer).

show abstract

Direct electrochemical measurement of nitric oxide in vascular endothelium

Cited by 86 publications

References 24 publications

Role of Membrane Potential and Expression of Endothelial Factors in Restenosis After Angioplasty in SHR

Role of Membrane Potential and Expression of Endothelial Factors in Restenosis After Angioplasty in SHR

Signaling-mediated Functional Activation of Inducible Nitric-oxide Synthase and Its Role in Stimulating Platelet Activation

Redox regulation of calcium ion channels: Chemical and physiological aspects

Contact Info

Product

Resources

About