Simultaneous Measurements of Ca
            <sup>2+</sup>
            and Nitric Oxide in Bradykinin-Stimulated Vascular Endothelial Cells

Blatter, Lothar A.; Taha, Ziad; Mesároš, Štefan; Shacklock, Philip S.; Wier, W. Gil; Maliński, Tadeusz

doi:10.1161/01.res.76.5.922

Cited by 109 publications

(58 citation statements)

References 11 publications

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“…Time courses of AA and NO release, and their absolute concentrations, have been set in agreement with literature [37,58].…”

Section: Discussionsupporting

confidence: 75%

“…NO release is dependent on eNOS activation: based on the model suggested by our group in these cells [17], eNOS, in addition to the canonical calcium-dependence, can be activated by AA. To account for this double regulation, and fitting the time course of NO increase experimentally measured using fluorescent probes and selective electrodes [17,37], we described NO production as follows (see Fig. 3F)…”

Section: Aa-activated Channel (Aaac)mentioning

confidence: 99%

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A Tridimensional Model of Proangiogenic Calcium Signals in Endothelial Cells

Munaron

2009

TOBIOJ

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Angiogenic factors, including bFGF and VEGF, induce cytosolic calcium (Ca c ) increases in endothelial cells, critically involved in angiogenesis progression. At low agonist concentrations, Ca c elevation is mainly due to calcium entry controlled by a complex interplay between two intracellular messengers, arachidonic acid (AA) and nitric oxide (NO), released upon stimulation with proangiogenic factors: they trigger spatially localized calcium signals restricted to the cell periphery, and such a spatiotemporal pattern could contribute to the specificity of cellular responses.Based on experimental measurements, here we provide the first quantitative spatiotemporal 3D modeling of proangiogenic calcium events in endothelial cells using Virtual Cell framework. The main aims were to validate previously proposed signaling pathways and to suggest new experimental protocols.The most relevant conclusions are: 1. The interplay between AA and NO, previously proposed to be responsible for VEGF/bFGF-dependent calcium entry in endothelial cells, triggers peripheral calcium signals that reproduce the experimental measurements; 2. Spatial restriction is not an artefact due to the calcium-sensitive dye; 3. Channels clusterization in thin lamellipodia plays a key role in the generation of the peripheral-restricted proangiogenic calcium signals; 4. A model containing two distinct channels, named AAAC and NOAC, respectively activated by AA or NO, explains the basic properties of proangiogenic calcium signals.This could be considered an 'open model' containing the simplest conditions leading to a satisfactory reproduction of the experimental results: it should be implemented in order to make it more complete and to maximize physical and biochemical constraints.

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“…Time courses of AA and NO release, and their absolute concentrations, have been set in agreement with literature [37,58].…”

Section: Discussionsupporting

confidence: 75%

Section: Aa-activated Channel (Aaac)mentioning

confidence: 99%

A Tridimensional Model of Proangiogenic Calcium Signals in Endothelial Cells

Munaron

2009

TOBIOJ

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“…In the cultured endothelial cells, shear stress caused by laminar flow of perfusate (0.02-1 Pa) induced NO release 3 to 5 sec after the initiation of flow (42). Bradykinininduced NO was detected 8 sec after the addition of bradykinin (43). Although the basic performance of the NO sensor and the experimental condition are different between their and our studies, the rapid response of the endothelial cells to shear stress and agonists was consistently observed in their in vitro study and in this in vivo study.…”

Section: Resultsmentioning

confidence: 98%

Evaluation of bioavailability of nitric oxide in coronary circulation by direct measurement of plasma nitric oxide concentration

Neishi

Mochizuki²,

Miyasaka³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Although bioavailability of NO in the coronary circulation is commonly evaluated by acetylcholine (ACh)-induced vasodilation, a change in plasma NO concentration and its relation to the flow response after injection of ACh are still unknown. Thus, we directly measured the concentration of NO in the coronary sinus by using a catheter-type NO sensor for coronary sinus. An NO-sensitive sensor was located and fixed in a 4-Fr catheter with a soft tip for protection of vascular wall. After calibration with an NO-saturated pure water, the catheter-type NO sensor was located in the coronary sinus in anesthetized dogs. The coronary flow velocity (CFV) was measured with a Doppler guide wire. Intracoronary injection of ACh (0.4 and 1.0 g͞kg) increased plasma NO concentration in a dose-dependent manner (3-10 nM). Although ACh increased CFV by 95%, there was no significant difference between the two ACh doses. After ACh, the peak value of plasma NO concentration was observed significantly later than CFV. N G -methyl-L-arginine (NO synthase inhibitor) decreased basal NO concentration by 3 nM and suppressed the ACh-induced NO synthesis with no significant change in average peak velocity. We conclude that production of NO in the coronary circulation can be evaluated in the coronary sinus. Although ACh increases both CFV and NO concentration, CFV dose not reflect NO concentration in terms of magnitude and time course. Direct measurement of plasma NO concentration by the catheter-type NO sensor is useful to evaluate bioavailability of NO in the coronary circulation.nitric oxide synthase ͉ nitric oxide-selective sensor ͉ acetylcholine ͉ coronary blood flow ͉ endothelial function N itric oxide (NO) released by endothelial cells is formed from L-arginine by nitric oxide synthase (NOS) (1). NO release is augmented by mechanical stimulation such as shear stress (2-6), pulsatile flow (7, 8), and axial strain (9). Such mechanical stresses, which are produced by the periodic myocardial contraction and relaxation, directly influence the coronary blood vessels, acting as an overwhelmingly dominant factor of the coronary blood flow regulation (10-12). Under the stimulatory influences by the mechanical stresses, coronary endothelial cells produce NO on a beat-to-beat basis (13). In the coronary circulation, endothelium-derived NO plays fundamental roles in the regulation of blood flow, exerting a tonic vasodilator influence at rest and with increasing myocardial metabolism (14).However, bioavailability of NO is diminished in the subjects with a wide range of cardiac risk factors and pathologic conditions, such as aging, gender, smoking, hypertension, hypercholesterolemia, diabetes mellitus, hyperhomocystinemia, heart failure, infections, and polymorphisms of the endothelial NOS (15-23). Importantly, endothelial dysfunction, characterized by decreased bioavailability of NO, is a predictor of cardiovascular risk and outcome (24-28).Several techniques have been used to evaluate the endothelial function or bioavailability of NO (29). Coronary en...

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“…Endothelium-dependent vasodilation also occurs with bradykinin (BK), mainly by the activation of bradykinin B 2 receptors. BK has been shown to increase the release of prostacyclin and NO from bovine aortic endothelial cells in culture (Busse et al, 1994;Blatter et al, 1995) and to produce hyperpolarization in coronary arteries with intact endothelium (Vanhoutte, 1993;Fisslthaler et al, 1999). The involvement of three major pathways, i.e.…”

Section: Introductionmentioning

confidence: 99%

Signal transduction pathways involved in kinin B₂ receptor‐mediated vasodilation in the rat isolated perfused kidney

Bagaté

Grima

Imbs

et al. 2001

British J Pharmacology

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1 The signal transduction pathways involved in kinin B 2 receptor-related vasodilation were investigated in rat isolated perfused kidneys. During prostaglandin F 2a or KCl-induced constriction, the vasodilator response to a selective B 2 receptor agonist, Tyr(Me) BK by more than 60%, while inhibition of the cannabinoid CB 1 receptor (SR 141716A) had only a moderate eect. 5 Acetylcholine induced a concentration-dependent relaxation with characteristics nearly similar to the response to Tyr(Me) 8 BK. In contrast, the relaxation elicited by sodium nitroprusside was potentiated in the absence of NO (L-NOARG or removal of endothelium) but remained unchanged otherwise. 6 These results indicate that the activation of kinin B 2 receptors in the rat isolated kidney elicits an endothelium-dependent vasorelaxation, mainly dependent on the activation of charybdotoxinsensitive Ca 2+ -activated K + channels. In addition, cytochrome P450 derivatives appear to be involved.

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Simultaneous Measurements of Ca ²⁺ and Nitric Oxide in Bradykinin-Stimulated Vascular Endothelial Cells

Cited by 109 publications

References 11 publications

A Tridimensional Model of Proangiogenic Calcium Signals in Endothelial Cells

A Tridimensional Model of Proangiogenic Calcium Signals in Endothelial Cells

Evaluation of bioavailability of nitric oxide in coronary circulation by direct measurement of plasma nitric oxide concentration

Signal transduction pathways involved in kinin B₂ receptor‐mediated vasodilation in the rat isolated perfused kidney

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Simultaneous Measurements of Ca 2+ and Nitric Oxide in Bradykinin-Stimulated Vascular Endothelial Cells

Cited by 109 publications

References 11 publications

A Tridimensional Model of Proangiogenic Calcium Signals in Endothelial Cells

A Tridimensional Model of Proangiogenic Calcium Signals in Endothelial Cells

Evaluation of bioavailability of nitric oxide in coronary circulation by direct measurement of plasma nitric oxide concentration

Signal transduction pathways involved in kinin B2 receptor‐mediated vasodilation in the rat isolated perfused kidney

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Product

Resources

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Simultaneous Measurements of Ca ²⁺ and Nitric Oxide in Bradykinin-Stimulated Vascular Endothelial Cells

Signal transduction pathways involved in kinin B₂ receptor‐mediated vasodilation in the rat isolated perfused kidney