Apoptosis induction by nitric oxide in adult cardiomyocytes via cGMP-signaling and its impairment after simulated ischemia

Taimor, Gerhild; Hofstaetter, Bettina; Piper, Hans Michael

doi:10.1016/s0008-6363(99)00272-2

Cited by 97 publications

(82 citation statements)

References 21 publications

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“…Similar rates were given in other experimental MI studies. [27][28][29] In our study both in the 2 nd and 28 th day, the most intensive apoptosis was determined in the border zone of infarct. Palojoki et al reported that apoptosis in the border zone continues until the 12 th week.…”

Section: Discussionsupporting

confidence: 45%

“…Although the effects of NO on apoptosis have been evaluated in many studies, the results of these studies were controversial. [26][27][28][29] However, NO mediated effects of nebivolol on apoptosis after MI has not been investigated before.…”

Section: Discussionmentioning

confidence: 99%

“…NO is known to have both apoptotic and anti-apoptotic effects [26][27][28][29]45,46 NO, synthesized by iNOS stimulated by the cytokines was shown to stimulate apoptosis. [26][27][28] The toxic effects of high concentrations of NO have been reported to be mediated by the formation of ONOO -. 29 The NO synthesized by eNOS, however, shows anti-apoptotic effects in the myocardium.…”

Section: Discussionmentioning

confidence: 99%

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The Effects of Nebivolol on Apoptosis in a Rat Infarct Model

Mercanoğlu

Safran

Güngör

et al. 2007

Circ J

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fter myocardial infarction (MI), a series of structural changes (expansion and thinning of the infracted area) occur. 1,2 Although these changes help to maintain the cardiac function at the early phase of MI, when they are not controlled, it might lead to left ventricular (LV) dysfunction. 3 Cellular and molecular mechanisms contributing to the LV dysfunction are not fully understood, apoptosis, both in the infarct and healthy myocardium has been shown as an important role. 4,5 Nebivolol, a selective -blocker, 6 was shown to improve the ventricular function and hemodynamic parameters in patients with LV dysfunction. In addition to -blocker activity, nebivolol regulates the releasing nitric oxide (NO) by the activation of endothelial NO synthase (e-NOS) in endothelial cells. NO is related not only to the maintenance of healthy endothelial function, but also to apoptosis.In the present study our aim is to evaluate the NO mediated effects of nebivolol after MI in rats and the role of antiapoptotic mechanisms in this effect. Methods Animal Groups, Dose Selection and Study DurationAnimals were housed in a temperature-controlled animal facility with a 12-h light/dark cycle, with tap water and rodent chow ad libitum and handled in accordance with the Guide for the Care and the Use of Laboratory Animals published by the US National Institutes of Health. All experimental procedures were approved by the Institutional Animal Ethic Committee of Istanbul University Experimental Medical Research Institute.Twelve-week-old male Sprague Dawley rats, with a mean weight of 250-300 g, were divided in 3 groups of 12 each: sham operated control (sham-control), MI induced (MI-control) and nebivolol treated (MI-nebivolol).Nebivolol was administrated within 10 min of reperfusion at dose of 0.1 mg/kg iv and continued orally at dose of 2.0 mg/kg, by gastric gavage once daily for 28 days. The iv dose of nebivolol was selected as the minimum -blocker dose (absence of significant effect on blood pressure and heart rate (HR)), after a preliminary dose-response study, (using 0.1-0.5-1 mg/kg of nebivolol iv) according to Sacco et al (Fig 1). 7 The oral dose was selected according to Sanchez et al. 8 Hemodynamic effects of these 2 dose regimes were compared with metoprolol, a 1-selective adrenoreceptor antagonist (Tables 1,2).To evaluate the effects of nebivolol on the apoptosis both in acute and sub-acute period of MI, time intervals were selected as 2 days (for acute) and 28 days (for sub-acute) of Background In the present study, nitric oxide (NO) was investigated to see if it mediated effects of nebivolol on apoptosis in the rat myocardial infarction (MI) model. Methods and ResultsRats were divided into 3 groups: sham operated (sham-control), MI-induced (MI-control) and nebivolol treated (MI-nebivolol). The initial dose of nebivolol was administrated intravenously (iv) within 10 min of post-MI reperfusion and continued orally for 28 days. NO mediated effects of nebivolol were assessed either in the early (2 nd day) or sub-acute (28 th day) ...

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Section: Discussionsupporting

confidence: 45%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Effects of Nebivolol on Apoptosis in a Rat Infarct Model

Mercanoğlu

Safran

Güngör

et al. 2007

Circ J

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“…Therapeutic intervention showing antioxidant or free radical scavenging activity should exert beneficial effects against oxidative stress associated with various cardiovascular diseases (CVDs) [27]. Possible mechanisms of tincture of Crataegus (TCR) include preventing the increase in lipid peroxidation and activity of marker enzymes, preventing the isoproterenol-induced decrease in antioxidant enzymes in the heart, and increasing the rate of ADP-stimulated oxygen uptake and respiratory coupling ratio in isoproterenol-induced rats [28].…”

Section: Cardiovascular Effectmentioning

confidence: 99%

Effect ofCrataegusUsage in Cardiovascular Disease Prevention: An Evidence-Based Approach

Wang

Xiong

Feng

2013

Evidence-Based Complementary and Alternative Medicine

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Hawthorn (Crataegus oxyacantha) is a widely used Chinese herb for treatment of gastrointestinal ailments and heart problems and consumed as food. In North America, the role of treatment for heart problems dates back to 1800. Currently, evidence is accumulating from various in vivo and in vitro studies that hawthorn extracts exert a wide range of cardiovascular pharmacological properties, including antioxidant activity, positive inotropic effect, anti-inflammatory effect, anticardiac remodeling effect, antiplatelet aggregation effect, vasodilating effect, endothelial protective effect, reduction of smooth muscle cell migration and proliferation, protective effect against ischemia/reperfusion injury, antiarrhythmic effect, lipid-lowering effect and decrease of arterial blood pressure effect. On the other hand, reviews of placebo-controlled trials have reported both subjective and objective improvement in patients with mild forms of heart failure (NYHA I–III), hypertension, and hyperlipidemia. This paper discussed the underlying pharmacology mechanisms in potential cardioprotective effects and elucidated the clinical applications of Crataegus and its various extracts.

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“…[93,94] In some cells, the pro-death signaling is initiated by cGMP, [95,96] while in others (including hepatocytes) cGMP inhibits apoptosis. [37,97,98] …”

Section: Chemical Fate Of No• In Biological Systemsmentioning

confidence: 99%