Nitric Oxide Activity Is Deficient in Spasm Arteries of Patients With Coronary Spastic Angina

Kugiyama, Kiyotaka; Yasue, Hirofumi; Okumura, Ken; Ogawa, Hisao; Fujimoto, Kazuteru; Nakao, Kōichi; Yoshimura, Michihiro; Motoyama, Takeshi; Inobe, Yoshito; Kawano, Hiroaki

doi:10.1161/01.cir.94.3.266

Cited by 339 publications

(209 citation statements)

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“…[19][20][21][22][23] Microparticles can also influence endothelial functions: microparticles from patients with acute coronary syndromes directly impaired endothelium-dependent vasodilatation in rat aorta rings, presumably by inhibition of the nitric oxidemediated signal transduction. 9,10 Although microparticles are elevated in condition of endothelial 24 Endothelial cell dysfunction may be detected clinically by measuring impairment of endotheliumdependent vasodilation 25 or by determining the plasma levels of circulating soluble markers. 26 These methods, however, are either relatively nonspecific, complicated or operator-dependent.…”

Section: Discussionmentioning

confidence: 99%

Endothelial microparticles correlate with erectile dysfunction in diabetic men

et al. 2006

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Cell-derived microparticles are supposed to be involved in endothelial dysfunction and atherogenesis. This study aimed to evaluate circulating microparticles in diabetic subjects with erectile dysfunction (ED) and their relation with endothelial dysfunction. Thirty diabetic men with ED and 20 age-matched control subjects without ED were assessed for circulating microparticles and endothelial dysfunction. Flow cytometry was used to assess microparticles by quantification of circulating endothelial (EMP, CD31 þ /CD42b À ) and platelet (PMP, CD31 þ /CD42b þ ) microparticles in peripheral blood. Endothelium-dependent flow-mediated dilation (FMD) was evaluated in the right brachial artery after reactive hyperemia. Compared with non-diabetic subjects, diabetic men presented significantly higher numbers of EMP (P ¼ 0.001), and reduced FMD (P ¼ 0.01), with a significant inverse correlation between the number of circulating EMP and the International Index of Erectile Function (IIEF) score (r ¼ À0.457, P ¼ 0.01). Multivariate analysis correcting for age, anthropometric indices, glucose and lipid parameters, FMD and PMP identified EMP as the only independent predictor for IIEF score (P ¼ 0.03). EMP are elevated in impotent diabetic subjects and independently involved in the pathogenesis of ED.

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Section: Discussionmentioning

confidence: 99%

Endothelial microparticles correlate with erectile dysfunction in diabetic men

et al. 2006

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“…Importantly, endothelial dysfunction, characterized by decreased bioavailability of NO, is a predictor of cardiovascular risk and outcome (24)(25)(26)(27)(28).…”

Section: N Itric Oxide (No) Released By Endothelial Cells Is Formed Frommentioning

confidence: 99%

“…In patients with risk factors for atherosclerosis and in those with coronary artery disease, infusion of ACh results in a diminished vasodilatory response or paradoxical vasoconstriction (30)(31)(32)(33)(34)(35). In spasm arteries of patients with coronary spastic angina, activity of NO is deficient (28,29). Although endothelium-dependent vasodilation has been commonly evaluated by intracoronary injection of ACh, there are still many uncertainties remaining in relation to the bioavailability of NO.…”

Section: N Itric Oxide (No) Released By Endothelial Cells Is Formed Frommentioning

confidence: 99%

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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“…They considered vascular dysfunction at level of the endothelium and/or smooth muscle as a possible cause of spasm at the myocardial bridge. Endothelial dysfunction (23) and/or dysfunction of smooth muscle cells (24) is thought to be involved in the genesis of coronary spasm. Ishii et al (25) have demonstrated that endothelial cells and smooth muscle cells are preserved beneath the myocardial bridge, but not in the segment proximal and distal to the myocardial bridge.…”

Section: Editorialmentioning

confidence: 99%