Vasodilating β-adrenoceptor blockers as cardiovascular therapeutics

Toda, Noboru

doi:10.1016/j.pharmthera.2003.09.001

Cited by 86 publications

(75 citation statements)

References 254 publications

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“…These results are in agreement with Tedesco et al [32]; Mancia et al [33]; Polónia et al [34]; Xiaozhen et al [35]; Erdoğan et al [36]. Reduction in arterial blood pressure by carvedilol may be attributed to it blocks norepinephrine binding to α1-adrenergic receptors in addition to both β1-adrenergic and β2-adrenergic receptors [37]. This results in a reduction in arterial blood pressure by maintaining cardiac output and decreasing total β-adrenergic vasoconstrictor tone [38].…”

Section: Discussionsupporting

confidence: 85%

“…This results in a reduction in arterial blood pressure by maintaining cardiac output and decreasing total β-adrenergic vasoconstrictor tone [38]. The presence of β2-adrenoceptor antagonism may also be of importance because of a potential role in the presynaptic modulation of catecholamine release [37] Table 3: Effects of administration of carvedilol, melatonin or carvedilol plus melatonin on parameters of free radicals and antioxidants in rats. Data represent mean ± S.E.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Combination of Carvedilol and Melatonin on Induced Metabolic Syndrome in Rats

Malak¹

2014

Biochem Physiol

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Background: The prevalence of metabolic syndrome is increasing and it is considered one of the main threats to human health worldwide. Fructose feeding induces hyper-insulinemia, insulin resistance and hyper-triglyceridemia. The main objective of the present study is to evaluate the pharmacological effects of the single and combined administration of carvedilol and melatonin on fructose-induced metabolic syndrome in rats.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Effects of Combination of Carvedilol and Melatonin on Induced Metabolic Syndrome in Rats

Malak¹

2014

Biochem Physiol

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“…In contrast, third-generation agents, such as nebivolol and carvedilol, possess vasodilator actions through such proposed mechanisms as NO release, antioxidant effects, β 2 agonism, and calcium blockade [108,109]. These vasodilating agents have beneficial or neutral effects on insulin sensitivity and glycemic control [82,[109][110][111].…”

Section: Mechanismsmentioning

confidence: 99%

Treating hypertension while protecting the vulnerable islet in the cardiometabolic syndrome

Hayden

Sowers

2008

Journal of the American Society of Hypertension

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Hypertension, a multifactorial-polygenic disease, interacts with multiple environmental stressors and results in functional and structural changes in numerous end organs, including the cardiovascular system. This can result in coronary heart disease, stroke, peripheral vascular disease, congestive heart failure, end-stage renal disease, insulin resistance, and damage to the pancreatic islet. Hypertension is the most important modifiable risk factor for major health problems encountered in clinical practice. Whereas hypertension was once thought to be a medical condition based on discrete blood pressure readings, a new concept has emerged defining hypertension as part of a complex and progressive metabolic and cardiovascular disease, an important part of a cardiometabolic syndrome. The central role of insulin resistance, oxidative stress, endothelial dysfunction, metabolic signaling defects within tissues, and the role of enhanced tissue renin-angiotensin-aldosterone system activity as it relates to hypertension and type 2 diabetes mellitus is emphasized. Additionally, this review focuses on the effect of hypertension on functional and structural changes associated with the vulnerable pancreatic islet. Various classes of antihypertensive drugs are reviewed, especially their roles in delaying or preventing damage to the vulnerable pancreatic islet, and thus delaying the development of type 2 diabetes mellitus.

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“…106 Celiprolol was suggested to be potentially useful in patients with angina pectoris and hypertension, complicated by other conditions associated with advanced age, impaired glucose tolerance or diabetes mellitus, peripheral vascular disease, and hyperlipidemia. 107,108 Coronary flow reserve at rest was less in patients with CAD than in control individuals; intracoronary administration of nebivolol increased coronary flow reserve both in the controls and patients; collateral flow index decreased with nebivolol and correlated to changes in heart rate.…”

Section: Angiotensin II Type 1 Receptor Blocker (Arb)mentioning

confidence: 99%

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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Vasodilating β-adrenoceptor blockers as cardiovascular therapeutics

Cited by 86 publications

References 254 publications

Effects of Combination of Carvedilol and Melatonin on Induced Metabolic Syndrome in Rats

Effects of Combination of Carvedilol and Melatonin on Induced Metabolic Syndrome in Rats

Treating hypertension while protecting the vulnerable islet in the cardiometabolic syndrome

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

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