Differential Effects of Calcium-Channel Blockers on Vascular Endothelial Function in Patients With Coronary Spastic Angina

Miwa, Yohei; Masai, Hiroyuki; Shimizu, Masatoshi

doi:10.1253/circj.cj-08-0188

Cited by 27 publications

(16 citation statements)

References 31 publications

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“…18 CCBs are recommended for vascular endothelial function in patients with coronary spastic angina. 19 However, conventional therapy was insufficient to treat recurrent chest pain in the MB patients. We did not find any correlation between medical therapy and modification of the outcome of MB, but additional use of aspirin or statin was useful for MB and lowered the readmission rate in those refractory to conventional medical therapy (CCB, BB).…”

Section: Kim Ss Et Almentioning

confidence: 99%

Long-Term Clinical Course of Patients With Isolated Myocardial Bridge

Kim

Jeong

Kim

et al. 2010

Circ J

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Section: Kim Ss Et Almentioning

confidence: 99%

Long-Term Clinical Course of Patients With Isolated Myocardial Bridge

Kim

Jeong

Kim

et al. 2010

Circ J

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“…Patients with coronary vasospasm had lower endothelium-dependent flow-mediated vasodilatation as compared with normal individuals; benidipine, but not diltiazem and verapamil, increased flow-mediated vasodilatation and plasma cyclic GMP levels; none of the treatments affected GTNinduced vasodilatation, suggesting that upregulation of the NO-cyclic GMP system by benidipine may partly contribute to the improvement of endothelial dysfunction. 121 Short-term (4 weeks) trimetazidine therapy improved heart rate variability parameters and endothelial products such as NO and ET-1 as well as anginal symptom in patients with slow coronary artery flow; this improvement was correlated with increased NO and decreased ET-1 levels. 122 The Rho kinase inhibitor fasudil increased endothelium-dependent vasodilatation in patients with CAD but not in healthy controls and also reduced Rho kinase activity in the patients, suggesting that inhibition of the Rho/Rho kinase pathway appears to provide a useful strategy to restore NO bioavailability in humans with atherosclerosis.…”

Section: Herbal Agentsmentioning

confidence: 93%

Nitric Oxide-Mediated Coronary Flow Regulation in Patients with Coronary Artery Disease: Recent Advances

Toda¹,

Tanabe²,

Nakanishi³

2011

Int J Angiol

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Nitric oxide (NO) formed via endothelial NO synthase (eNOS) plays crucial roles in the regulation of coronary blood flow through vasodilatation and decreased vascular resistance, and in inhibition of platelet aggregation and adhesion, leading to the prevention of coronary circulatory failure, thrombosis, and atherosclerosis. Endothelial function is impaired by several pathogenic factors including smoking, chronic alcohol intake, hypercholesterolemia, obesity, hyperglycemia, and hypertension. The mechanisms underlying endothelial dysfunction include reduced NO synthase (NOS) expression and activity, decreased NO bioavailability, and increased production of oxygen radicals and endogenous NOS inhibitors. Atrial fibrillation appears to be a risk factor for endothelial dysfunction. Endothelial dysfunction is an important predictor of coronary artery disease (CAD) in humans. Penile erectile dysfunction, associated with impaired bioavailability of NO produced by eNOS and neuronal NOS, is also considered to be highly predictive of ischemic heart disease. There is evidence suggesting an important role of nitrergic innervation in coronary blood flow regulation. Prophylactic and therapeutic measures to eliminate pathogenic factors inducing endothelial and nitrergic nerve dysfunction would be quite important in preventing the genesis and development of CAD.KEYWORDS: Nitric oxide, constitutive nitric oxide synthase, endothelial dysfunction, coronary blood flow, coronary artery disease, asymmetric dimethylarginine Coronary blood flow is regulated through complex adjustments in the arteriolar tone and resistance of the microcirculation. Impairment of microvascular function leads to organ dysfunction in any body system including the heart. Recent evidence supports the concept that the impairment of endothelial function is an upstream event in the pathophysiology of atherosclerosis, CAD, and myocardial infarction (MI). Nitric oxide (NO) liberated as a paracrine relaxant from the vascular endothelium is known to play a pivotal role in the modulation of microvascular tone and regional blood flow.1 In addition, NO inhibits platelet aggregation and adhesion, inhibits leukocyte adhesion and migration, and reduces vascular smooth muscle proliferation, thus leading to prevention of atherosclerosis. NO produced via neuronal NO synthase (nNOS) is released from Abundant and varied data from animal and human studies, performed over the course of more than two decades, indicate that depression of synthesis and bioavailability of NO in the endothelium participates in many cardiovascular diseases, including atherosclerosis, 4 coronary heart diseases, 5 stroke, 3 renal failure, 6 and hypertension 5,7 and also in insulin resistance and diabetes mellitus.8 Mechanisms underlying impairment of NO-mediated vasodilatation and blood flow increase include the downregulation of endothelial NOS (eNOS) and nNOS expressions, generation of NOS inhibitors and NO scavengers, and upregulation of vasoconstrictor substances, such as endothelin-1 (ET-1),...

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“…Another Dihydropyridine benidipine (Coniel), which also blocks both LTCC and TTCC, had a similar beneficial effect on vascular endothelium (Miwa et al 2009), and benidipine hydrochloride also appears the most preferable antihypertensive for patients with diabetes. Here, it is more effective in lowering blood pressure than amlodipine or cilnidipine and it also has an additional renal-protective effect (Seino et al 2007;Ohishi et al 2007).…”

Section: Dihydropyridinesmentioning

confidence: 99%

Pharmacology of Voltage-Gated Calcium Channels in Clinic

Lacinová

Lichvarova

2013

Pathologies of Calcium Channels

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The diversity of voltage-gated calcium channels (VGCC) allows precise time-and voltage-dependent regulation of calcium ions entry into cells. Individual calcium channel subtypes participate in the initiation of neuronal action potential and repetitive action potential firing; in cardiac pacemaking and signal conduction; in shaping an action potential plateau; and in action potential repolarization. Calcium entry through VGCC is necessary for cardiac and smooth muscle cell contraction. Since disrupted regulation of calcium homeostasis accompanies various pathologies, the complex pattern of regulation of cell physiology by VGCC makes them an attractive target for pharmaceutical agents. The most common pathologies treated with VGCC blockers are cardiovascular diseases, especially hypertension, angina, and tachycardia. In addition, calcium channels have been identified as targets of some antiepileptic and anesthetic drugs. More recently, specific VGCC blockers were introduced in the treatment of chronic pain, and these have also proved beneficial as support therapy in neurodegenerative diseases and cognitive impairment. IntroductionVoltage-gated calcium channels (VGCC) are a family of voltage-gated ion channels which are far less diverse than the voltage-gated potassium channel family-in respect to the number of representatives and also to the diversity of the current waveform. It is, however, much more diverse than the voltage-gated sodium channel family in respect to its kinetics and voltage dependencies of channel gating. Since the calcium current is ionic, it flows through the VGCC and modulates the dynamics

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Differential Effects of Calcium-Channel Blockers on Vascular Endothelial Function in Patients With Coronary Spastic Angina

Cited by 27 publications

References 31 publications

Long-Term Clinical Course of Patients With Isolated Myocardial Bridge

Long-Term Clinical Course of Patients With Isolated Myocardial Bridge

Nitric Oxide-Mediated Coronary Flow Regulation in Patients with Coronary Artery Disease: Recent Advances

Pharmacology of Voltage-Gated Calcium Channels in Clinic

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