Effects of Antihypertensive Drugs on Alcohol-Induced Functional Responses of Cultured Human Endothelial Cells

Soardo, Giorgio; Donnini, Debora; Moretti, Massimo; Milocco, C.; Catena, Cristiana; Sechi, Leonardo Antonio

doi:10.1291/hypres.31.345

Cited by 13 publications

(9 citation statements)

References 42 publications

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“…The fact that propranolol, a beta-blocker with no anti-oxidant activity, is non-protective and, as alluded to earlier, the amelioration of both ROS production and EMP generation by carvedilol, support the hypothesis that the protective effect of the latter is mediated through its anti-oxidant effect. This is also consistent with the previous findings of carvedilol being able to increase intracellular glutathione and reduce malondialdehyde production with alcohol-induced oxidative stress in human endothelial cells [36], and block lipid peroxidation in epinephrine-treated human coronary-artery endothelial cells [35]. …”

Section: Discussionsupporting

confidence: 93%

Carvedilol Protects against Iron-Induced Microparticle Generation and Apoptosis of Endothelial Cells

et al. 2014

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Background: Increased circulating endothelial microparticles (EMPs) have been shown to associate with endothelial dysfunction. We explored the effect of iron on EMP generation by human umbilical vein endothelial cells (HUVECs) and the potential protective effect of carvedilol. Methods: FeCl₃ was added to HUVEC culture. Iron entry into cells was monitored using fluorescent microscopic imaging, while the quantity of EMPs that was released was determined by flow cytometry. The apoptosis of HUVECs was assessed by annexin V/propidium iodide assay and caspase-3 expression. Membrane bleb formation was visualized using electron microscopy. Intracellular production of reactive oxygen species (ROS) was also monitored. The effects of beta-blockers, carvedilol and propranolol on these processes were determined by co-incubation in a dose-dependent manner. Iron entry into HUVECs was not blocked by either beta-blocker. Iron induced the generation of EMPs, the formation of membrane blebs, the apoptosis of HUVECs and the production of ROS, each in a dose-dependent manner. Carvedilol, but not propranolol, ameliorated all of these processes. Results: Our result indicates that iron induces EMP generation and apoptosis of endothelial cells in association with increased oxidative stress. Conclusion: The protective effects of carvedilol, via its antioxidant effect, may have therapeutic potential in patients with iron overload.

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Section: Discussionsupporting

confidence: 93%

Carvedilol Protects against Iron-Induced Microparticle Generation and Apoptosis of Endothelial Cells

et al. 2014

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“…The serum levels of vasoactive substances such as reninaldosterone have been reported to be affected by alcohol ingestion in vivo or ethanol in vitro [54][55][56] . Antihypertensive drugs are shown to offer protection against alcohol induced responses in cultured human endothelial cells suggesting the possible involvement of renin-angiotensin system (RAS) [56] .…”

Section: Renin-angiotensin-aldosterone System In Alcohol-induced Hypementioning

confidence: 99%

“…Antihypertensive drugs are shown to offer protection against alcohol induced responses in cultured human endothelial cells suggesting the possible involvement of renin-angiotensin system (RAS) [56] . It has been reported that a significant increase in plasma renin activity in patients consuming heavy alcohol compared to mild or moderate alcohol consumption [55,57,58] .…”

Section: Renin-angiotensin-aldosterone System In Alcohol-induced Hypementioning

confidence: 99%

Alcohol-induced hypertension: Mechanism and prevention

Husain¹,

Ansari²,

Ferder³

2014

WJC

260

194

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Epidemiological, preclinical and clinical studies established the association between high alcohol consumption and hypertension. However the mechanism through which alcohol raises blood pressure remains elusive. Several possible mechanisms have been proposed such as an imbalance of the central nervous system, impairment of the baroreceptors, enhanced sympathetic activity, stimulation of the renin-angiotensin-aldosterone system, increased cortisol levels, increased vascular reactivity due to increase in intracellular calcium levels, stimulation of the endothelium to release vasoconstrictors and loss of relaxation due to inflammation and oxidative injury of the endothelium leading to inhibition of endothelium-dependent nitric oxide production. Loss of relaxation due to inflammation and oxidative injury of the endothelium by angiotensin II leading to inhibition of endothelium-dependent nitric oxide production is the major contributors of the alcohol-induced hypertension. For the prevention of alcohol-induced hypertension is to reduce the amount of alcohol intake. Physical conditioning/exercise training is one of the most important strategies to prevent/treat chronic alcohol-induced hypertension on physiological basis. The efficacious pharmacologic treatment includes the angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (ARBs) which have antioxidant activity and calcium channel blockers. The most effective prevention and treatment of alcohol-induced hypertension is physical exercise and the use of ACE inhibitors or ARBs in the clinic.

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“…The improved endothelial activity and vascular function associated with vasodilating beta-blockers (particularly nebivolol) is believed to be mediated via nitric oxidedependent pathways [19,48,50,51], specifically, an increase in nitric oxide bioavailability and a decrease in oxidative stress. Recent experimental data using a nanotechnological approach to simultaneously monitor nitric oxide and peroxynitrite (ONOO À ) in aortic endothelial cells from Wistar-Kyoto rats have confirmed that endothelial nitric oxide synthase (eNOS) uncoupling is observed with aging, manifested by a three-fold decrease in nitric oxide and a three-fold increase in ONOO À [52].…”

Section: Potential Mechanisms Underlying Central Hemodynamic Effects mentioning

confidence: 99%

What is the role, if any, for beta-blockers as initial therapy for uncomplicated hypertension?

Pedersen

Cockcroft²

2009

Current Opinion in Cardiology

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The majority of evidence suggesting that beta-blockade should not be used in uncomplicated hypertension comes from studies using atenolol. It would therefore be premature and unwise to eliminate all beta-blockers from the array of agents available to optimize BP control in patients with uncomplicated hypertension by extrapolating data based almost entirely on the conventional beta-blocker atenolol. Vasodilating beta-blockers have beneficial effects on central BP, arterial stiffening, and nitric oxide-dependent endothelial dysfunction that may contribute to their clinical benefits in patients with hypertension.

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Effects of Antihypertensive Drugs on Alcohol-Induced Functional Responses of Cultured Human Endothelial Cells

Cited by 13 publications

References 42 publications

Carvedilol Protects against Iron-Induced Microparticle Generation and Apoptosis of Endothelial Cells

Carvedilol Protects against Iron-Induced Microparticle Generation and Apoptosis of Endothelial Cells

Alcohol-induced hypertension: Mechanism and prevention

What is the role, if any, for beta-blockers as initial therapy for uncomplicated hypertension?

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