Measurement of acetylcholine-induced endothelium-derived nitric oxide in aorta using a newly developed catheter-type nitric oxide sensor

Mochizuki, Seiichi; Miyasaka, Takehiro; Goto, Masami; Ogasawara, Yasuo; Yada, Toyotaka; Akiyama, Maki; Neishi, Yoji; Toyoda, Tomohiko; Tomita, Junko; Koyama, Yuji; Tsujioka, Katsuhiko; Kajiya, Fumihiko; Yoshida, Kiyoshi

doi:10.1016/s0006-291x(03)00985-9

Cited by 31 publications

(51 citation statements)

References 12 publications

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“…The mean sensitivity of the seven sensors used in the present study was 366 Ϯ 122 pA͞nM. In our previous study, prototype catheter-type NO sensors for the measurement in aorta, which used the same sensor as that used in this study, showed the sensitivity of 498 Ϯ 40 pA͞nM (seven sensors) (41). The mean sensitivity of the NO sensor for the coronary sinus was slightly lower than that of the NO sensor for the aorta.…”

Section: Resultsmentioning

confidence: 48%

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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Section: Resultsmentioning

confidence: 48%

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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“…[8][9][10] The NO sensors showed no noticeable change in response to oxygen, ACh, and solution mixing, indicating high specificity to NO (data not shown). The mean sensitivity of the 7 sensors used in the present study was 317±13 pA· nmol/L.…”

Section: Calibration Of Sensorsmentioning

confidence: 96%

“…[8][9][10] In brief, an NO sensor (amino-700 XL, Innovative Instruments, 700 m in diameter at the detection tip) was mounted in a 4-Fr catheter (1,200 mm long; Hirakawa Hewtech, Tokyo, Japan) and fixed with silicon adhesive. The oxidative current of NO was monitored by with an NO monitor (model inNO-T, Innovative Instruments).…”

Section: A Catheter Type No Sensormentioning

confidence: 99%

“…Each sensor was calibrated by using an NO-saturated pure water as previously described. [8][9][10] Briefly, NO-saturated pure water was prepared by bubbling pure NO gas in oxygen-free pure water. Using a gas-tight syrindge, 5 l was injected into a well Background We examined whether nitroglycerin (NTG)-induced impairment of nitric oxide (NO) bioavailability could be modified by a peroxisome proliferator-activated receptor (PPAR) agonist.…”

Section: A Catheter Type No Sensormentioning

confidence: 99%

“…Using a gas-tight syrindge, 5 l was injected into a well stirred saline solution (50 ml) in which the NO sensor was immersed (final NO concentration: 190 nmol/L) as previously described. [8][9][10] The baseline (zero level) is set arbitrarily in the amperometric method, and thus, a peak change in the current form from the baseline is used and is expressed as 'change in NO concentration (nmol/L)' because NO concentration cannot be measured as an absolute value with the amperometric method. [8][9][10] …”

Section: A Catheter Type No Sensormentioning

confidence: 99%

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Effect of Pioglitazone on Nitroglycerin-Induced Impairment of Nitric Oxide Bioavailability by a Catheter-Type Nitric Oxide Sensor

Ikejima

Imanishi

Tsujioka

et al. 2008

Circ J

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everal clinical and basic studies have shown that chronic treatment with nitroglycerin (NTG) causes endothelial dysfunction. [1][2][3] However, the limitation of these data is that the release of nitric oxide (NO) from the endothelium was estimated on the basis of the comparison of vessel relaxation. We have very recently shown that longterm treatment of New Zealand White rabbits with NTG decreases basal, as well as acetylcholine (ACh)-induced plasma NO concentrations by using a catheter-type NO sensor, accompanied with augmentation of nitrosative stress. 4 In addition, we have shown that the negative effects of NTG could be prevented by co-treatment with drugs attenuating nitrosative stress, such as, angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor blockers (ARB). 4 The peroxisome proliferator-activated receptor (PPAR) is a nuclear receptor that has recently emerged as a pivotal intracellular controller of systemic and vascular processes, including inflammation and atherosclerosis. 5 PPAR is expressed in all major cell types involved in the initiation and evolution of the atherosclerotic plaque, including endothelial cells, vascular smooth muscle cells, macrophages, and T lymphocytes, where it might exert anti-inflammatory and potentially anti-atherogenic effects. 6 Interestingly, PPAR stimulation improves insulin resistance as well as endothelial function in patients with type 2 diabetes. 7 However, it is unknown whether this beneficial effect of PPAR stimulation on endothelial function could extend to NTG-induced endothelial dysfunction. It is clinically important because patients with diabetes mellitus have frequently accompanied with ischemic heart disease.By using the catheter-type NO sensor we investigated to clarify the effect of PPAR agonist on the impairment of bioavailability of NO induced by chronic treatment with NTG patches. The present study has shown that the NTGinduced impairment of NO bioavailability is significantly reversed by the co-treatment with a PPAR agonist, pioglitazone. Methods A Catheter Type NO SensorIntegrated architecture and performance of the cathetertype NO sensor have been described previously. [8][9][10] In brief, an NO sensor (amino-700 XL, Innovative Instruments, 700 m in diameter at the detection tip) was mounted in a 4-Fr catheter (1,200 mm long; Hirakawa Hewtech, Tokyo, Japan) and fixed with silicon adhesive. The oxidative current of NO was monitored by with an NO monitor (model inNO-T, Innovative Instruments). Each sensor was calibrated by using an NO-saturated pure water as previously described. [8][9][10] Briefly, NO-saturated pure water was prepared by bubbling pure NO gas in oxygen-free pure water. Using a gas-tight syrindge, 5 l was injected into a well Background We examined whether nitroglycerin (NTG)-induced impairment of nitric oxide (NO) bioavailability could be modified by a peroxisome proliferator-activated receptor (PPAR) agonist. Methods and ResultsMale New Zealand White rabbits were treated for 7 days with NTG patches, either al...

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Transport Limitations of Nitric Oxide Inhibition of Platelet Aggregation under Flow

et al. 2013

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Nitric oxide (NO) inhibits platelet aggregation at and near the site of a vascular injury by upregulation of cyclic guanosine monophosphate, which reduces the dimerization of the integrin α(IIb)β₃. The magnitude of NO flux from the vessel wall and the NO concentration that is necessary to inhibit platelet aggregation under physiological flow conditions is unknown. In this study, a NO releasing polymer, diazeniumdiolated dibutylhexanediamine, was integrated into a microfluidic flow assay to determine the relationship between NO wall flux and collagen mediated platelet adhesion, activation and aggregation. A NO flux equal to or greater than 2.5 × 10⁻¹⁰ mol cm⁻² min⁻¹ was found to abrogate aggregation, but not initial platelet adhesion, on collagen at 200 and 500 s⁻¹ as effectively as the α(IIb)β₃ antagonist abciximab. The dynamic range of NO fluxes found to induce measurable inhibition of platelet aggregation spanned from 0.33 × 10⁻¹⁰ to 2.5 × 10⁻¹⁰ mol cm⁻² min⁻¹ at 200-500 s⁻¹. These fluxes correspond to near-wall NO concentrations of 3-90 nM based on a computational model of NO transport. The model predicts that NO concentration in the platelet rich layer near the wall is kinetically limited, while NO penetration into the lumen is mass transfer limited.

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Measurement of acetylcholine-induced endothelium-derived nitric oxide in aorta using a newly developed catheter-type nitric oxide sensor

Cited by 31 publications

References 12 publications

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

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

Effect of Pioglitazone on Nitroglycerin-Induced Impairment of Nitric Oxide Bioavailability by a Catheter-Type Nitric Oxide Sensor

Transport Limitations of Nitric Oxide Inhibition of Platelet Aggregation under Flow

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