Effects of propranolol on heart muscle mitochondria

Sakurada, Asae; Voss, Dinor O.; Brandão, Dorei; Campello, Annibal P.

doi:10.1016/0006-2952(72)90327-9

Cited by 30 publications

(14 citation statements)

References 18 publications

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“…There is a significant lack of literature of the propranolol mode of action in autotrophic organisms, though heterotrophic and autotrophic model organisms are very different, in terms of mitochondrial transporters these are highly conserved between organisms, and thus some comparisons at this level can be made to disclose some of the possible mechanisms of this molecule at the mitochondrial level. In heterotrophs, propranolol is known to inhibit mitochondrial electron transport [78][79][80]. In rat cardiac tissue the NADH-oxidase, NADH-cytochrome c reductase and heart inner membrane mitochondrial transporters activity were depressed by propranolol [80].…”

Section: Discussionmentioning

confidence: 99%

Effects of Propranolol on Growth, Lipids and Energy Metabolism and Oxidative Stress Response of Phaeodactylum tricornutum

Duarte

Feijão

Carvalho

et al. 2020

Biology

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Present demographic trends suggest a rise in the contributions of human pharmaceuticals into coastal ecosystems, underpinning an increasing demand to evaluate the ecotoxicological effects and implications of drug residues in marine risk assessments. Propranolol, a non-selective β-adrenoceptor blocker, is used worldwide to treat high blood pressure conditions and other related cardiovascular conditions. Although diatoms lack β-adrenoceptors, this microalgal group presents receptor-like kinases and proteins with a functional analogy to the animal receptors and that can be targeted by propranolol. In the present work, the authors evaluated the effect of this non-selective β-adrenoceptor blocker in diatom cells using P. tricornutum as a model organism, to evaluate the potential effect of this compound in cell physiology (growth, lipids and energy metabolism and oxidative stress) and its potential relevance for marine ecosystems. Propranolol exposure leads to a significant reduction in diatom cell growth, more evident in the highest concentrations tested. This is likely due to the observed impairment of the main primary photochemistry processes and the enhancement of the mitochondrial respiratory activity. More specifically, propranolol decreased the energy transduction from photosystem II (PSII) to the electron transport chain, leading to an increase in oxidative stress levels. Cells exposed to propranolol also exhibited high-dissipated energy flux, indicating that this excessive energy is efficiently diverted, to some extent, from the photosystems, acting to prevent irreversible photoinhibition. As energy production is impaired at the PSII donor side, preventing energy production through the electron transport chain, diatoms appear to be consuming storage lipids as an energy backup system, to maintain essential cellular functions. This consumption will be attained by an increase in respiratory activity. Considering the primary oxygen production and consumption pathways, propranolol showed a significant reduction of the autotrophic O2 production and an increase in the heterotrophic mitochondrial respiration. Both mechanisms can have negative effects on marine trophic webs, due to a decrease in the energetic input from marine primary producers and a simultaneous oxygen production decrease for heterotrophic species. In ecotoxicological terms, bio-optical and fatty acid data appear as highly efficient tools for ecotoxicity assessment, with an overall high degree of classification when these traits are used to build a toxicological profile, instead of individually assessed.

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Section: Discussionmentioning

confidence: 99%

Effects of Propranolol on Growth, Lipids and Energy Metabolism and Oxidative Stress Response of Phaeodactylum tricornutum

Duarte

Feijão

Carvalho

et al. 2020

Biology

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“…However, it has been shown that, at the subcellular level, propranolol reduces mitochondrial respiration by inhibition of NADH oxidase (29) and inhibits Ca 2+ uptake by isolated sarcoplasmic reticulum (30).…”

Section: Reimer Rasmussen Jenningsmentioning

confidence: 99%

Reduction by Propranolol of Myocardial Necrosis following Temporary Coronary Artery Occlusion in Dogs

Reimer

Rasmussen

Jennings

1973

Circulation Research

206

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The effect of propranolol on the severity of myocardial necrosis following 40 minutes of temporary coronary artery occlusion was assessed in dogs. The circumflex coronary artery was occluded 1-2 cm from the aorta in open-chest dogs anesthetized with sodium pentobarbital. One group of dogs was untreated and a second group received propranolol (5.0 mg/kg, iv) 10 minutes prior to the occlusion. After 40 minutes the clamp was removed and arterial perfusion was restored. Dogs which survived this procedure were killed 2-5 days later for gross and histologic assessment of the necrosis. The relative area of necrosis (percent of fibers involved) in the posterior papillary muscle of each heart was quantified from stained histologic sections prepared from serial longitudinal slices of each posterior papillary muscle. Dogs treated with propranolol showed significantly less necrosis than did untreated controls, but the mechanism of the drug's action remains unknown. During coronary artery occlusion, propranolol-treated dogs exhibited somewhat lower heart rates, systolic blood pressures , and S-T segment elevations than did untreated dogs. However, none of these latter differences between groups was significant. KEY WORDS infarction heart quantification of infarct size ventricular fibrillation cell death ^8-receptor blockade S-T segment elevation • In the past few years much attention has been directed toward various therapeutic interventions which slow or prevent the development of myocar-dial cell death following an acute coronary artery occlusion. Sommers and Jennings (1) have suggested that propranolol in some way alters the course of ischemic injury.-They observed that 17 of 31 untreated dogs subjected to a 20-minute temporary occlusion of the circumflex coronary artery showed foci of necrosis 24-48 hours later. Only 3 of 30 similar dogs treated prophylactically with proprano-lol showed any necrosis. The 20-minute occlusion, however, induced relatively mild injury even without treatment, since it caused only small islands of cell death in about half of the untreated dogs. The present study was undertaken to provide a more severe test of propranolol's efficacy against myocardial ischemic injury. A 40-minute period of temporary circumflex coronary artery occlusion was chosen for study; injury induced by this method causes necrosis in 100% of dogs in the absence of protective therapy, and the characteristics of this model have been described in considerable detail (2, 3). The posterior papillary muscle is in the center of the lesion and is the site of maximum, most predictable injury. The proportion of muscle fibers which become necrotic can readily be quantified and in a previous series of dogs was about 55% of the posterior papillary muscle projecting above the endocardial surface of the ventricle (4). Thus this model provides an appropriate injury in which either beneficial or deleteri-ous interventions can be observed. In this study our purpose was to determine whether propranolol could reduce the number of cells which ...

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“…We take the opportunity of Presedo's comments to reiterate that our patients were all free from any medication, beta-blockers included, at the time of study. This was clearly stated in both our papers (1, 2) (p. 477 (1) and p. 263 (2) "all patients examined were free from chronic ergotism and any medi-cations"); medication of any kind was withdrawn at least one month before examinations. So we feel confident that our findings relate to a true basal state of the patients.…”

Section: Dear Sirmentioning

confidence: 58%