Статті в журналах: "Β1-Blockers"

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Bennett, Miriam, Catherina L. Chang, Michael Tatley, Ruth Savage та Robert J. Hancox. "The safety of cardioselective β1-blockers in asthma: literature review and search of global pharmacovigilance safety reports". ERJ Open Research 7, № 1 (січень 2021): 00801–2020. http://dx.doi.org/10.1183/23120541.00801-2020.

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IntroductionBeta-blockers are key in the management of cardiovascular diseases but blocking airway β2-receptors can cause severe and sometimes fatal bronchoconstriction in people with asthma. Although cardioselective β1-blockers may be safer than non-selective β-blockers, they remain relatively contraindicated and under-prescribed. We review the evidence of the risk associated with cardioselective β1-blocker use in asthma.MethodsWe searched “asthma” AND “beta-blocker” in PubMed and EmbaseOvid from start to May 2020. The World Health Organization (WHO) global database of individual case safety reports (VigiBase) was searched for reports of fatal asthma or bronchospasm and listed cardioselective β1-blocker use (accessed February 2020). Reports were examined for evidence of pre-existing asthma.ResultsPubMed and EmbaseOvid searches identified 304 and 327 publications, respectively. No published reports of severe or fatal asthma associated with cardioselective β1-blockers were found. Three large observational studies reported no increase in asthma exacerbations with cardioselective β1-blocker treatment. The VigiBase search identified five reports of fatalities in patients with pre-existing asthma and reporting asthma or bronchospasm during cardioselective β1-blocker use. Four of these deaths were unrelated to cardioselective β1-blocker use. The circumstances of the fifth death were unclear.ConclusionsThere were no published reports of cardioselective β1-blockers causing asthma death. Observational data suggest that cardioselective β1-blocker use is not associated with increased asthma exacerbations. We found only one report of an asthma death potentially caused by cardioselective β1-blockers in a patient with asthma in a search of VigiBase. The reluctance to use cardioselective β1-blockers in people with asthma is not supported by this evidence.

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do Vale, Gabriel T., Carla S. Ceron, Natália A. Gonzaga, Janaina A. Simplicio та Júlio C. Padovan. "Three Generations of β-blockers: History, Class Differences and Clinical Applicability". Current Hypertension Reviews 15, № 1 (29 січня 2019): 22–31. http://dx.doi.org/10.2174/1573402114666180918102735.

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Background: Beta-adrenergic receptors are expressed in cardiomyocytes and activated by either noradrenaline released from sympathetic synapses or circulating catecholamines. Their corresponding receptors have three subtypes, namely, β1, β2 and β3, which are members of the G protein-coupled receptors (GPCRs) family. Activation of β1-adrenergic receptors causes various physiological reactions including cardiac contraction and renin secretion from juxtaglomerular cells of the kidney. Antagonists of β-adrenergic receptors, known as β-blockers, have been used effectively for over four decades and have beneficial effects in the treatment of cardiovascular diseases. There are three generations of β-blockers according to their pharmacological properties. Firstgeneration β-blockers are non-selective, blocking both β1- and β2-receptors; second-generation β- blockers are more cardioselective in that they are more selective for β1-receptors; and thirdgeneration β-blockers are highly selective drugs for β1-receptors. The latter also display vasodilator actions by blocking α1-adrenoreceptors and activating β3-adrenergic receptors. In addition, thirdgeneration β-blockers exhibit angiogenic, antioxidant, anti-proliferative, anti-hypertrophic and antiapoptotic activities among other effects that are still under investigation. Conclusion: The objective of this review is to describe the evolution observed during the development of the three distinctive generations, thereby highlighting the advantages of third-generation β- blockers over the other two drug classes.

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Karoli, N. A., and A. P. Rebrov. "Possibilities and limitations of the use of beta-blockers in patients with cardiovascular disease and chronic obstructive pulmonary disease." Kardiologiia 61, no. 10 (October 30, 2021): 89–98. http://dx.doi.org/10.18087/cardio.2021.10.n1119.

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In medical literature, increasing attention is paid to comorbidities in patients with chronic obstructive pulmonary disease (COPD). In clinical practice, physicians often hesitate to prescribe beta-blockers (β1-adrenoblockers) to COPD patients. This article summarized new results of using beta-blockers in patients with COPD. According to reports, the selective β1-blocker treatment considerably increases the survival rate of patients with COPD and ischemic heart disease, particularly after myocardial infarction (MI), and with chronic heart failure (CHF). The benefit of administering selective β1-blockers to patients with CHF and/or a history of MI overweighs a potential risk related with the treatment even in patients with severe COPD. Convincing data in favor of the β1-blocker treatment in COPD patients without the above-mentioned comorbidities are not available. At present, the selective β1-blocker treatment is considered safe for patients with cardiovascular diseases and COPD. For this reason, selective β1-blockers, such as bisoprolol, metoprolol or nebivolol can be used in managing this patient cohort. Nonselective β1-blockers may induce bronchospasm and are not recommended for COPD patients. For the treatment with β-blockers with intrinsic sympathomimetic activity, the probability of bronchial obstruction in COPD patients is lower; however, drugs of this pharmaceutical group have not been compared with cardioselective beta-blockers. For safety reasons, the beta-blocker treatment should be started outside exacerbation of COPD and from a small dose. Careful monitoring is recommended for possible new symptoms, such as emergence/increase of shortness of breath, cough or changes in dosing of other drugs (for example, increased frequency of using short-acting bronchodilators).

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Stănciulescu, Maria-Corina, Marius-Călin Popoiu, Anca Maria Cîmpean, Vlad-Laurentiu David, Rodica Heredea, Simona Cerbu та Eugen-Sorin Boia. "Expression of β1 adrenergic receptor in vascular anomalies in children". Journal of International Medical Research 49, № 9 (вересень 2021): 030006052110477. http://dx.doi.org/10.1177/03000605211047713.

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Objective Controversial, heterogeneous, and inconsistent responses to beta-blockers have been reported in some cases of infantile proliferative hemangiomas. On the basis of these clinical observations, we aimed to examine the β1 adrenergic receptor (β1-AR) protein expression distribution among different types of pediatric vascular anomalies. Methods Immunohistochemistry (IHC) was performed for β1-AR on 43 surgical specimens. Results We found positive β1-AR IHC staining in all intramuscular hemangiomas, capillary–lymphatic, lymphatic, venous, and combined malformations, and Masson’s tumor cases, as well as in 7 of 10 cases of proliferative infantile hemangiomas. Conclusions Our research demonstrates, for the first time, the degree of heterogeneous expression of β1-AR among pediatric vascular malformations. Our results support the need for β1-AR assessment in pediatric vascular anomalies to select cases with a robust response to β1-selective blockers. β1-AR assessment may have a strong impact on therapeutic refinement for pediatric vascular anomalies by selecting cases with a stronger response to beta-blockers.

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Barcella, Carlo A., Talip E. Eroglu, Michiel Hulleman, Asger Granfeldt, Patrick C. Souverein, Grimur H. Mohr, Rudolph W. Koster, et al. "Association of beta-blockers and first-registered heart rhythm in out-of-hospital cardiac arrest: real-world data from population-based cohorts across two European countries." EP Europace 22, no. 8 (June 28, 2020): 1206–15. http://dx.doi.org/10.1093/europace/euaa124.

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Abstract Aims Conflicting results have been reported regarding the effect of beta-blockers on first-registered heart rhythm in out-of-hospital cardiac arrest (OHCA). We aimed to establish whether the use of beta-blockers influences first-registered rhythm in OHCA. Methods and results We included patients with OHCA of presumed cardiac cause from two large independent OHCA-registries from Denmark and the Netherlands. Beta-blocker use was defined as exposure to either non-selective beta-blockers, β1-selective beta-blockers, or α-β-dual-receptor blockers within 90 days prior to OHCA. We calculated odds ratios (ORs) for the association of beta-blockers with first-registered heart rhythm using multivariable logistic regression. We identified 23 834 OHCA-patients in Denmark and 1584 in the Netherlands: 7022 (29.5%) and 519 (32.8%) were treated with beta-blockers, respectively. Use of non-selective beta-blockers, but not β1-selective blockers, was more often associated with non-shockable rhythm than no use of beta-blockers [Denmark: OR 1.93, 95% confidence interval (CI) 1.48–2.52; the Netherlands: OR 2.52, 95% CI 1.15–5.49]. Non-selective beta-blocker use was associated with higher proportion of pulseless electrical activity (PEA) than of shockable rhythm (OR 2.38, 95% CI 1.01–5.65); the association with asystole was of similar magnitude, although not statistically significant compared with shockable rhythm (OR 2.34, 95% CI 0.89–6.18; data on PEA and asystole were only available in the Netherlands). Use of α-β-dual-receptor blockers was significantly associated with non-shockable rhythm in Denmark (OR 1.21; 95% CI 1.03–1.42) and not significantly in the Netherlands (OR 1.37; 95% CI 0.61–3.07). Conclusion Non-selective beta-blockers, but not β1-selective beta-blockers, are associated with non-shockable rhythm in OHCA.

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Grande, Fedora, Anna De Bartolo, Maria Antonietta Occhiuzzi, Anna Caruso, Carmine Rocca, Teresa Pasqua, Alessia Carocci, Vittoria Rago, Tommaso Angelone та Maria Stefania Sinicropi. "Carbazole and Simplified Derivatives: Novel Tools toward β-Adrenergic Receptors Targeting". Applied Sciences 11, № 12 (13 червня 2021): 5486. http://dx.doi.org/10.3390/app11125486.

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β-Adrenergic receptors (β-ARs) are G protein-coupled receptors involved in important physiological and pathological processes related to blood pressure and cardiac activity. The inhibition of cardiac β1-ARs could be beneficial in myocardial hypertrophy, ischemia and failure. Several carbazole-based compounds have been described as promising β-blockers. Herein, we investigate the capability of a carbazole derivative and three simplified indole analogs to interact with the active binding site of β1-AR by molecular docking studies. In the light of the obtained results, our compounds were tested by biological assays in H9c2 cardiomyocytes exposed to isoproterenol (ISO) to confirm their potential as β1-blockers agents, and two of them (8 and 10) showed interesting and promising properties. In particular, these compounds were effective against ISO-dependent in vitro cardiac hypertrophy, even at concentrations lower than the known β-AR antagonist propranolol. Overall, the data suggest that the indole derivatives 8 and 10 could act as potent β1-blockers and, active at low doses, could elicit limited side effects.

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Artym, Vira V., та Howard R. Petty. "Molecular Proximity of Kv1.3 Voltage-gated Potassium Channels and β1-Integrins on the Plasma Membrane of Melanoma Cells". Journal of General Physiology 120, № 1 (10 червня 2002): 29–37. http://dx.doi.org/10.1085/jgp.20028607.

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Tumor cell membranes have multiple components that participate in the process of metastasis. The present study investigates the physical association of β1-integrins and Kv1.3 voltage-gated potassium channels in melanoma cell membranes using resonance energy transfer (RET) techniques. RET between donor-labeled anti–β1-integrin and acceptor-labeled anti-Kv1.3 channels was detected on LOX cells adherent to glass and fibronectin-coated coverslips. However, RET was not observed on LOX cells in suspension, indicating that molecular proximity of these membrane molecules is adherence-related. Several K+ channel blockers, including tetraethylammonium, 4-aminopyridine, and verapamil, inhibited RET between β1-integrins and Kv1.3 channels. However, the irrelevant K+ channel blocker apamin had no effect on RET between β1-integrins and Kv1.3 channels. Based on these findings, we speculate that the lateral association of Kv1.3 channels with β1-integrins contributes to the regulation of integrin function and that channel blockers might affect tumor cell behavior by influencing the assembly of supramolecular structures containing integrins.

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Singh, Bramah N. "β-Adrenergic Blockers as Antiarrhythmic and Antifibrillatory Compounds: An Overview". Journal of Cardiovascular Pharmacology and Therapeutics 10, № 4_suppl (жовтень 2005): S3—S14. http://dx.doi.org/10.1177/10742484050100i402.

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β-Adrenergic blockers have a wide spectrum of action for controlling cardiac arrhythmias that is larger than initially thought. Data from the past several decades indicate that, as an antiarrhythmic class, β-blockers remain among the very few pharmacologic agents that reduce the incidence of sudden cardiac death, prolong survival, and ameliorate symptoms caused by arrhythmias in patients with cardiac disease. As a class of compounds, β-blockers have a fundamental pharmacologic property that attenuates the effects of competitive adrenergic receptors. However, the net clinical effects of the different β-receptor blockers may vary quantitatively because of variations in associated intrinsic sympathomimetic agonism and in their intrinsic potency for binding to β-receptors. These individual compounds also differ in their selectivity for β1- and β2-receptors. Metoprolol is a β1-selective blocker, whereas carvedilol is a nonselective β1- and β2-blocker, an antioxidant, and has a propensity to inhibit α1-receptors and endothelin. Evolving data from controlled and uncontrolled clinical trials suggest that there are clinically significant differences among this class of drugs. Recent evidence also suggests that the antiarrhythmic actions of certain β-receptor blockers such as carvedilol and metoprolol extend beyond the ventricular tissue to encompass atrial cells and help maintain sinus rhythm in patients with atrial fibrillation, especially in combination with potent antifibrillatory agents such as amiodarone. This introduction provides a current perspective on these newer developments in the understanding of the antiarrhythmic and antifibrillatory actions of β-blockers.

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Winther, K., and C. Hedman. "Beta-Adrenoceptor Blockade, Platelets, and Rheologic Factors." Cephalalgia 6, no. 5_suppl (May 1986): 33–40. http://dx.doi.org/10.1177/03331024860060s504.

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Alterations in platelet function and other hemorheologic factors have been reported to occur in patients with migraine. The prophylactic treatment of migraine with beta blockers is at present well established, and non-selective as well as β1-selective beta blockers exert an effect. The aim of this presentation is to summarize how beta blockers, depending on their receptor selectivity, modulate platelet function and hemorheologic factors. We conclude that nonselective beta blockade increases factors, such as platelet aggregability, and decreases fibrinolytic activity compared with β1-selective blockade with metoprolol. These differences do not reflect on their migraine prophylactic effect and indicate that alterations in platelet function are not a primary cause of migraine: rather, they are epiphenomena.

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Diniz, Gabriela Placoná, Marcela Sorelli Carneiro-Ramos та Maria Luiza Morais Barreto-Chaves. "Thyroid Hormone Increases TGF-β1 in Cardiomyocytes Cultures Independently of Angiotensin II Type 1 and Type 2 Receptors". International Journal of Endocrinology 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/384890.

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TH-induced cardiac hypertrophyin vivois accompanied by increased cardiac Transforming Growth Factor-β1 (TGF-β1) levels, which is mediated by Angiotensin II type 1 receptors (AT1R) and type 2 receptors (AT2R). However, the possible involvement of this factor in TH-induced cardiac hypertrophy is unknown. In this study we evaluated whether TH is able to modulate TGF-β1 in isolated cardiac, as well as the possible contribution of AT1R and AT2R in this response. The cardiac fibroblasts treated withT3did not show alteration on TGF-β1 expression. However, cardiomyocytes treated withT3presented an increase in TGF-β1 expression, as well as an increase in protein synthesis. The AT1R blockade prevented theT3-induced cardiomyocyte hypertrophy, while the AT2R blockage attenuated this response. TheT3-induced increase on TGF-β1 expression in cardiomyocytes was not changed by the use of AT1R and AT2R blockers. These results indicate that Angiotensin II receptors are not implicated inT3-induced increase on TGF-βexpression and suggest that the trophic effects exerted byT3on cardiomyocytes are not dependent on the higher TGF-β1 levels, since the AT1R and AT2R blockers were able to attenuate theT3-induced cardiomyocyte hypertrophy but were not able to attenuate the increase on TGF-β1 levels promoted byT3.

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Clemente-Moragón, Agustín, Mónica Gómez, Rocío Villena-Gutiérrez, Doménica V. Lalama, Jaime García-Prieto, Fernando Martínez, Fátima Sánchez-Cabo, Valentín Fuster, Eduardo Oliver, and Borja Ibáñez. "Metoprolol exerts a non-class effect against ischaemia–reperfusion injury by abrogating exacerbated inflammation." European Heart Journal 41, no. 46 (October 7, 2020): 4425–40. http://dx.doi.org/10.1093/eurheartj/ehaa733.

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Abstract Aims Clinical guidelines recommend early intravenous β-blockers during ongoing myocardial infarction; however, it is unknown whether all β-blockers exert a similar cardioprotective effect. We experimentally compared three clinically approved intravenous β-blockers. Methods and results Mice undergoing 45 min/24 h ischaemia–reperfusion (I/R) received vehicle, metoprolol, atenolol, or propranolol at min 35. The effect on neutrophil infiltration was tested in three models of exacerbated inflammation. Neutrophil migration was evaluated in vitro and in vivo by intravital microscopy. The effect of β-blockers on the conformation of the β1 adrenergic receptor was studied in silico. Of the tested β-blockers, only metoprolol ameliorated I/R injury [infarct size (IS) = 18.0% ± 0.03% for metoprolol vs. 35.9% ± 0.03% for vehicle; P < 0.01]. Atenolol and propranolol had no effect on IS. In the three exacerbated inflammation models, neutrophil infiltration was significantly attenuated only in the presence of metoprolol (60%, 50%, and 70% reductions vs. vehicle in myocardial I/R injury, thioglycolate-induced peritonitis, and lipopolysaccharide-induced acute lung injury, respectively). Migration studies confirmed the particular ability of metoprolol to disrupt neutrophil dynamics. In silico analysis indicated different intracellular β1 adrenergic receptor conformational changes when bound to metoprolol than to the other two β-blockers. Conclusions Metoprolol exerts a disruptive action on neutrophil dynamics during exacerbated inflammation, resulting in an infarct-limiting effect not observed with atenolol or propranolol. The differential effect of β-blockers may be related to distinct conformational changes in the β1 adrenergic receptor upon metoprolol binding. If these data are confirmed in a clinical trial, metoprolol should become the intravenous β-blocker of choice for patients with ongoing infarction.

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Nuttall, S. L., H. C. Routledge та M. J. Kendall. "A comparison of the β1 -selectivity of three β1 -selective β-blockers". Journal of Clinical Pharmacy and Therapeutics 28, № 3 (червень 2003): 179–86. http://dx.doi.org/10.1046/j.1365-2710.2003.00477.x.

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WAJIMA, Zen'ichiro. "Future Possibilities for the Clinical Use of β1-blockers". JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA 26, № 4 (2006): 398–403. http://dx.doi.org/10.2199/jjsca.26.398.

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Nakaya, Michio, Satsuki Chikura, Kenji Watari, Natsumi Mizuno, Koji Mochinaga, Supachoke Mangmool, Satoru Koyanagi та ін. "Induction of Cardiac Fibrosis by β-Blocker in G Protein-independent and G Protein-coupled Receptor Kinase 5/β-Arrestin2-dependent Signaling Pathways". Journal of Biological Chemistry 287, № 42 (10 серпня 2012): 35669–77. http://dx.doi.org/10.1074/jbc.m112.357871.

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G-protein coupled receptors (GPCRs) have long been known as receptors that activate G protein-dependent cellular signaling pathways. In addition to the G protein-dependent pathways, recent reports have revealed that several ligands called “biased ligands” elicit G protein-independent and β-arrestin-dependent signaling through GPCRs (biased agonism). Several β-blockers are known as biased ligands. All β-blockers inhibit the binding of agonists to the β-adrenergic receptors. In addition to β-blocking action, some β-blockers are reported to induce cellular responses through G protein-independent and β-arrestin-dependent signaling pathways. However, the physiological significance induced by the β-arrestin-dependent pathway remains much to be clarified in vivo. Here, we demonstrate that metoprolol, a β1-adrenergic receptor-selective blocker, could induce cardiac fibrosis through a G protein-independent and β-arrestin2-dependent pathway. Metoprolol, a β-blocker, increased the expression of fibrotic genes responsible for cardiac fibrosis in cardiomyocytes. Furthermore, metoprolol induced the interaction between β1-adrenergic receptor and β-arrestin2, but not β-arrestin1. The interaction between β1-adrenergic receptor and β-arrestin2 by metoprolol was impaired in the G protein-coupled receptor kinase 5 (GRK5)-knockdown cells. Metoprolol-induced cardiac fibrosis led to cardiac dysfunction. However, the metoprolol-induced fibrosis and cardiac dysfunction were not evoked in β-arrestin2- or GRK5-knock-out mice. Thus, metoprolol is a biased ligand that selectively activates a G protein-independent and GRK5/β-arrestin2-dependent pathway, and induces cardiac fibrosis. This study demonstrates the physiological importance of biased agonism, and suggests that G protein-independent and β-arrestin-dependent signaling is a reason for the diversity of the effectiveness of β-blockers.

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Áblad, Bengt, та Carl Dahlöf. "Migraine and β-Blockade: Modulation of Sympathetic Neurotransmission". Cephalalgia 6, № 5_suppl (травень 1986): 7–14. http://dx.doi.org/10.1177/03331024860060s501.

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The pathophysiology of both classical and common migraine is still not understood, and there is controversy as to whether the origin is vascular, neuronal, or both. Although the mechanism for the prophylactic effect of β-blockers in migraine has not been elucidated yet, the therapeutic action of β1-blockers and non-selective β-blockers devoid of intrinsic activity is well established by many controlled trials. Mainly on the basis of data from animal experiments, the possible role of central β-adrenoceptor-mediated mechanisms involved in the control of the activity of noradrenergic neurons will be discussed with reference to migraine.

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Blaauw, Erik, Frans A. van Nieuwenhoven, Peter Willemsen, Tammo Delhaas, Frits W. Prinzen, Luc H. Snoeckx, Marc van Bilsen, and Ger J. van der Vusse. "Stretch-induced hypertrophy of isolated adult rabbit cardiomyocytes." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 3 (September 2010): H780—H787. http://dx.doi.org/10.1152/ajpheart.00822.2009.

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Both mechanical and humoral triggers have been put forward to explain the hypertrophic response of the challenged cardiomyocyte. The aim of the present study was to investigate whether cyclic equibiaxial stretch is a direct stimulus for isolated adult rabbit cardiomyocytes to develop hypertrophy and to explore the potential involvement of the autocrine/paracrine factors ANG II, transforming growth factor (TGF)-β1, and IGF-I in this process. Isolated cardiomyocytes were exposed to 10% cyclic equibiaxial stretch (1 Hz) for up to 48 h or treated with ANG II (100 nM), TGF-β1 (5 ng/ml), IGF-I (100 ng/ml), ANG II type 1 (AT1) receptor blockers, or conditioned medium of stretched fibroblasts. Cyclic stretch significantly increased cell surface area (+3.1%), protein synthesis (+21%), and brain natriuretic peptide (BNP) mRNA expression (6-fold) in cardiomyocytes. TGF-β1 expression increased (+42%) transiently at 4 h, whereas cardiomyocyte IGF-I expression was not detectable under all experimental conditions. The AT1 receptor blockers candesartan and irbesartan (100 nM) did not prevent the stretch-induced hypertrophic response. Direct exposure to ANG II, TGF-β1, or IGF-I did not enhance cardiomyocyte BNP expression. In cardiac fibroblasts, stretch elicited a significant approximately twofold increase in TGF-β1 and IGF-I expression. Conditioned medium of stretched fibroblasts increased BNP expression in cardiomyocytes (∼2-fold, P = 0.07). This study clearly indicates that cyclic stretch is a strong, direct trigger to induce hypertrophy in fully differentiated rabbit cardiomyocytes. The present findings do not support the notion that stretch-mediated hypertrophy of adult rabbit cardiomyocytes involves autocrine/paracrine actions of ANG II, TGF-β1, or IGF-I.

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Ashes, Catherine, Saul Judelman, Duminda N. Wijeysundera, Gordon Tait, C. David Mazer, Gregory M. T. Hare та W. Scott Beattie. "Selective β1-Antagonism with Bisoprolol Is Associated with Fewer Postoperative Strokes than Atenolol or Metoprolol". Anesthesiology 119, № 4 (1 жовтня 2013): 777–87. http://dx.doi.org/10.1097/aln.0b013e3182a17f12.

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Abstract Background: Perioperative metoprolol increases postoperative stroke. Animal studies indicate that the mechanism may be related to attenuated β2-adrenoreceptor-mediated cerebral vasodilatation. The authors therefore conducted a cohort to study whether the highly β1-specific β-blocker (bisoprolol) was associated with a reduced risk of postoperative stroke compared with less selective β-blockers (metoprolol or atenolol). Methods: The authors conducted a single-center study on 44,092 consecutive patients with age 50 yr or more having noncardiac, nonneurologic surgery. The primary outcome was stroke within 7 days of surgery. The secondary outcome was a composite of all-cause mortality, postoperative myocardial injury, and stroke. A propensity score-matched cohort was created to assess the independent association between bisoprolol and less β1-selective agents metoprolol or atenolol. A secondary analysis using logistic regression, based on previously identified confounders, also compared selective β1-antagonism. Results: Twenty-four percent (10,756) of patients were exposed to in-hospital β-blockers. A total of 88 patients (0.2%) suffered a stroke within 7 days of surgery. The matched cohort consisted of 2,462 patients, and the pairs were well matched for all variables. Bisoprolol was associated with fewer postoperative strokes than the less selective agents (odds ratio = 0.20; 95% CI, 0.04–0.91). Multivariable risk-adjustment in the β-blockers-exposed patients comparing bisoprolol with the less selective agents was associated with a similarly reduced stroke rate. Conclusions: The use of metoprolol and atenolol is associated with increased risks of postoperative stroke, compared with bisoprolol. These findings warrant confirmation in a pragmatic randomized trial.

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Peltenburg, Puck J., Dania Kallas, Johan M. Bos, Krystien V. V. Lieve, Sonia Franciosi, Thomas M. Roston, Isabelle Denjoy та ін. "An International Multicenter Cohort Study on β-Blockers for the Treatment of Symptomatic Children With Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation 145, № 5 (лютий 2022): 333–44. http://dx.doi.org/10.1161/circulationaha.121.056018.

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Background: Symptomatic children with catecholaminergic polymorphic ventricular tachycardia (CPVT) are at risk for recurrent arrhythmic events. β-Blockers decrease this risk, but studies comparing individual β-blockers in sizeable cohorts are lacking. We aimed to assess the association between risk for arrhythmic events and type of β-blocker in a large cohort of symptomatic children with CPVT. Methods: From 2 international registries of patients with CPVT, RYR2 variant–carrying symptomatic children (defined as syncope or sudden cardiac arrest before β-blocker initiation and age at start of β-blocker therapy <18 years), treated with a β-blocker were included. Cox regression analyses with time-dependent covariates for β-blockers and potential confounders were used to assess the hazard ratio (HR). The primary outcome was the first occurrence of sudden cardiac death, sudden cardiac arrest, appropriate implantable cardioverter-defibrillator shock, or syncope. The secondary outcome was the first occurrence of any of the primary outcomes except syncope. Results: We included 329 patients (median age at diagnosis, 12 [interquartile range, 7–15] years, 35% females). Ninety-nine (30.1%) patients experienced the primary outcome and 74 (22.5%) experienced the secondary outcome during a median follow-up of 6.7 (interquartile range, 2.8–12.5) years. Two-hundred sixteen patients (66.0%) used a nonselective β-blocker (predominantly nadolol [n=140] or propranolol [n=70]) and 111 (33.7%) used a β1-selective β-blocker (predominantly atenolol [n=51], metoprolol [n=33], or bisoprolol [n=19]) as initial β-blocker. Baseline characteristics did not differ. The HRs for both the primary and secondary outcomes were higher for β1-selective compared with nonselective β-blockers (HR, 2.04 [95% CI, 1.31–3.17]; and HR, 1.99 [95% CI, 1.20–3.30], respectively). When assessed separately, the HR for the primary outcome was higher for atenolol (HR, 2.68 [95% CI, 1.44–4.99]), bisoprolol (HR, 3.24 [95% CI, 1.47–7.18]), and metoprolol (HR, 2.18 [95% CI, 1.08–4.40]) compared with nadolol, but did not differ from propranolol. The HR of the secondary outcome was only higher in atenolol compared with nadolol (HR, 2.68 [95% CI, 1.30–5.55]). Conclusions: β1-selective β-blockers were associated with a significantly higher risk for arrhythmic events in symptomatic children with CPVT compared with nonselective β-blockers, specifically nadolol. Nadolol, or propranolol if nadolol is unavailable, should be the preferred β-blocker for treating symptomatic children with CPVT.

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Durgaryan, Ruzan. "C0159 β1 blockers, warfarin and rhythm conversion in atrial fibrillation". Thrombosis Research 130 (жовтень 2012): S173. http://dx.doi.org/10.1016/j.thromres.2012.08.188.

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Fedorov, V. N., V. P. Vdovichenko, M. K. Korsakov, V. V. Strakhov, A. A. Popova, A. I. Khokhlov, and S. S. Suleymanov. "Pharmacotherapy of glaucoma in terms of evidence-based medicine." Kachestvennaya Klinicheskaya Praktika = Good Clinical Practice, no. 3 (October 20, 2023): 44–54. http://dx.doi.org/10.37489/2588-0519-2023-3-44-54.

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Glaucoma is a disease associated with increased intraocular pressure (IOP). Of the pharmacological agents for treating glaucoma, there are drugs of the first (most effective and safe) and second-line treatment. First-line treatment includes prostaglandin analogs and beta-blockers. The currently used prostaglandin analogs (latanoprost, bimatoprost, tafluprost and travoprost) are PG F2α analogs that act through stimulation of FP receptors. They are distinguished by the optimal ratio of effectiveness and risk of side effects. They are convenient for the patient because for the therapeutic effect, it is enough to prescribe 1 time per day. As a result, it is rational to start the treatment of glaucoma with a drug in this group. In terms of pharmacoeconomics, the most affordable prostaglandin drug is latanoprost, which is generally as effective as other prostaglandin analogs. β-adrenergic blockers reduce the production of intraocular fluid, the formation of which is controlled by β1- and β2-adrenergic receptors. Therefore, non-selective β-blockers (timolol, levobunolol, metipranolol, and carteolol) have a pharmacodynamic advantage over selective β1-adrenergic antagonists (betaxolol). Conducted clinical studies of β-blockers have shown that given the cost, efficacy and safety, timolol was the most preferable treatment for glaucoma. In the presence of medical contraindications to the use of first-line drugs or to enhance their effectiveness, α2-agonists (apraclonidine and brimonidine), carbonic anhydrase inhibitors (usually local action: dorzolamide and brinzolamide), M-cholinomimetics (pilocarpine, carbachol and echothiopate), and also Rho-kinase inhibitors (ripasudil)

21

Geng, Yanyan, Xiaoyu Wang, and Karl L. Magleby. "Lack of negative slope in I-V plots for BK channels at positive potentials in the absence of intracellular blockers." Journal of General Physiology 141, no. 4 (March 25, 2013): 493–97. http://dx.doi.org/10.1085/jgp.201210955.

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Large-conductance, voltage- and Ca2+-activated K+ (BK) channels display near linear current–voltage (I-V) plots for voltages between −100 and +100 mV, with an increasing sublinearity for more positive potentials. As is the case for many types of channels, BK channels are blocked at positive potentials by intracellular Ca2+ and Mg2+. This fast block progressively reduces single-channel conductance with increasing voltage, giving rise to a negative slope in the I-V plots beyond about +120 mV, depending on the concentration of the blockers. In contrast to these observations of pronounced differences in the magnitudes and shapes of I-V plots in the absence and presence of intracellular blockers, Schroeder and Hansen (2007. J. Gen. Physiol. http://dx.doi.org/10.1085/jgp.200709802) have reported identical I-V plots in the absence and presence of blockers for BK channels, with both plots having reduced conductance and negative slopes, as expected for blockers. Schroeder and Hansen included both Ca2+ and Mg2+ in the intracellular solution rather than a single blocker, and they also studied BK channels expressed from α plus β1 subunits, whereas most previous studies used only α subunits. Although it seems unlikely that these experimental differences would account for the differences in findings between previous studies and those of Schroeder and Hansen, we repeated the experiments using BK channels comprised of α plus β1 subunits with joint application of 2.5 mM Ca2+ plus 2.5 mM Mg2+, as Schroeder and Hansen did. In contrast to the findings of Schroeder and Hansen of identical I-V plots, we found marked differences in the single-channel I-V plots in the absence and presence of blockers. Consistent with previous studies, we found near linear I-V plots in the absence of blockers and greatly reduced currents and negative slopes in the presence of blockers. Hence, studies of conductance mechanisms for BK channels should exclude intracellular Ca2+/Mg2+, as they can reduce conductance and induce negative slopes.

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Yi, Sheng, Fernando Pierucci-Alves та Bruce D. Schultz. "Transforming growth factor-β1 impairs CFTR-mediated anion secretion across cultured porcine vas deferens epithelial monolayer via the p38 MAPK pathway". American Journal of Physiology-Cell Physiology 305, № 8 (15 жовтня 2013): C867—C876. http://dx.doi.org/10.1152/ajpcell.00121.2013.

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The goal of this study was to determine whether transforming growth factor-β1 (TGF-β1) affects epithelial cells lining the vas deferens, an organ that is universally affected in cystic fibrosis male patients. In PVD9902 cells, which are derived from porcine vas deferens epithelium, TGF-β1 exposure significantly reduced short-circuit current ( Isc) stimulated by forskolin or a cell membrane-permeant cAMP analog, 8-pCPT-cAMP, suggesting that TGF-β1 affects targets of the cAMP signaling pathway. Electrophysiological results indicated that TGF-β1 reduces the magnitude of current inhibited by cystic fibrosis transmembrane conductance regulator (CFTR) channel blockers. Real-time RT-PCR revealed that TGF-β1 downregulates the abundance of mRNA coding for CFTR, while biotinylation and Western blot showed that TGF-β1 reduces both total CFTR and apical cell surface CFTR abundance. These results suggest that TGF-β1 causes a reduction in CFTR expression, which limits CFTR-mediated anion secretion. TGF-β1-associated attenuation of anion secretion was abrogated by SB431542, a TGF-β1 receptor I inhibitor. Signaling pathway studies showed that the effect of TGF-β1 on Isc was reduced by SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK). TGF-β1 exposure also increased the amount of phospho-p38 MAPK substantially. In addition, anisomycin, a p38 MAPK activator, mimicked the effect of TGF-β1, which further suggests that TGF-β1 affects PVD9902 cells through a p38 MAPK pathway. These observations suggest that TGF-β1, via TGF-β1 receptor I and p38 MAPK signaling, reduces CFTR expression to impair CFTR-mediated anion secretion, which would likely compound the effects associated with mild CFTR mutations and ultimately would compromise male fertility.

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Casabella-Ramón, Sergi, Verónica Jiménez-Sábado, Carmen Tarifa, Sandra Casellas, Tien Tina Lu, Paloma Izquierdo-Castro, Ignasi Gich та ін. "Impact of R-Carvedilol on β2-Adrenergic Receptor-Mediated Spontaneous Calcium Release in Human Atrial Myocytes". Biomedicines 10, № 7 (21 липня 2022): 1759. http://dx.doi.org/10.3390/biomedicines10071759.

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A hallmark of atrial fibrillation is an excess of spontaneous calcium release events, which can be mimicked by β1- or β2-adrenergic stimulation. Because β1-adrenergic receptor blockers (β1-blockers) are primarily used in clinical practice, we here examined the impact of β2-adrenergic stimulation on spontaneous calcium release and assessed whether the R- and S-enantiomers of the non-selective β- blocker carvedilol could reverse these effects. For this purpose, human atrial myocytes were isolated from patients undergoing cardiovascular surgery and subjected to confocal calcium imaging or immunofluorescent labeling of the ryanodine receptor (RyR2). Interestingly, the β2-adrenergic agonist fenoterol increased the incidence of calcium sparks and waves to levels observed with the non-specific β-adrenergic agonist isoproterenol. Moreover, fenoterol increased both the amplitude and duration of the sparks, facilitating their fusion into calcium waves. Subsequent application of the non β-blocking R-Carvedilol enantiomer reversed these effects of fenoterol in a dose-dependent manner. R-Carvedilol also reversed the fenoterol-induced phosphorylation of the RyR2 at Ser-2808 dose-dependently, and 1 µM of either R- or S-Carvedilol fully reversed the effect of fenoterol. Together, these findings demonstrate that β2-adrenergic stimulation alone stimulates RyR2 phosphorylation at Ser-2808 and spontaneous calcium release maximally, and points to carvedilol as a tool to attenuate the pathological activation of β2-receptors.

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Farhoumand, Lina S., Hongtao Liu, Theodora Tsimpaki, Ulrike B. Hendgen-Cotta, Tienush Rassaf, Nikolaos E. Bechrakis, Miltiadis Fiorentzis, and Utta Berchner-Pfannschmidt. "Blockade of ß-Adrenergic Receptors by Nebivolol Enables Tumor Control Potential for Uveal Melanoma in 3D Tumor Spheroids and 2D Cultures." International Journal of Molecular Sciences 24, no. 6 (March 20, 2023): 5894. http://dx.doi.org/10.3390/ijms24065894.

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Uveal melanoma (UM) is the most common primary cancer of the eye in adults. A new systemic therapy is needed to reduce the high metastasis and mortality rate. As β-blockers are known to have anti-tumor effects on various cancer entities, this study focuses on investigating the effect of β1-selective blockers atenolol, celiprolol, bisoprolol, metoprolol, esmolol, betaxolol, and in particular, nebivolol on UM. The study was performed on 3D tumor spheroids as well as 2D cell cultures, testing tumor viability, morphological changes, long-term survival, and apoptosis. Flow cytometry revealed the presence of all three β-adrenoceptors with a dominance of β2-receptors on cell surfaces. Among the blockers tested, solely nebivolol concentration-dependently decreased viability and altered 3D tumor spheroid structure. Nebivolol blocked the repopulation of cells spreading from 3D tumor spheroids, indicating a tumor control potential at a concentration of ≥20 µM. Mechanistically, nebivolol induced ATP depletion and caspase-3/7 activity, indicating that mitochondria-dependent signaling is involved. D-nebivolol or nebivolol combined with the β2-antagonist ICI 118.551 displayed the highest anti-tumor effects, suggesting a contribution of both β1- and β2-receptors. Thus, the present study reveals the tumor control potential of nebivolol in UM, which may offer a perspective for co-adjuvant therapy to reduce recurrence or metastasis.

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Wydra, Wioletta, and Marek Kuch. "Nebivolol – a place in the therapy of hypertension in various clinical situations." Medycyna Faktów 14, no. 2 (June 30, 2021): 195–200. http://dx.doi.org/10.24292/01.mf.0221.9.

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Nebivolol is a long-acting, most cardioselective β1-blocker. It stimulates endothelial production of nitric oxide, demonstrating vasodilatory and pleiotropic effects. It has better tolerance compared to classic β-blockers. It lowers the central pressure, reducing the risk of cardiovascular events. It is the preferred β-blocker in the treatment of hypertension in various clinical situations.

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Verdecchia, Paolo, Claudio Cavallini, Stefano Coiro, Clara Riccini та Fabio Angeli. "Certainties fading away: β-blockers do not worsen chronic obstructive pulmonary disease". European Heart Journal Supplements 23, Supplement_E (1 жовтня 2021): E172—E176. http://dx.doi.org/10.1093/eurheartj/suab116.

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Abstract For many years, β-blockers have been considered contraindicated in patients with heart failure (HF) and in those with bronchial asthma or even chronic obstructive pulmonary disease (COPD) although without clear evidence of asthma. Today, despite overwhelming evidence of the usefulness of β-blockers, especially in HF with reduced left ventricular ejection fraction (HFrEF), and in ischaemic heart disease, some reluctance persists in using these drugs when COPD coexists. Such resistance is due to the fear that a possible worsening of bronchospasm induced by β-blockers could induce negative effects greater than the benefits. The Guidelines of the European Society of Cardiology clearly suggest that: (i) implantation of a cardiac defibrillator (ICD) are not contraindicated in COPD without clear evidence of bronchial asthma; (ii) β-blockers are only ‘relatively’ contraindicated when there is certainty of bronchial asthma with a documented bronchodilator response to the β2 stimulant. Therefore, bronchial asthma is not an absolute contraindication to β-blockers. The cardiologist should not limit the diagnosis of COPD to clinical suspicion, but should rely on a spirometry examination associated with any bronchodilation tests. In any case, selective β1 blockers are preferred, starting at a basic dose, which ensure a better dilator response to bronchodilators and in any case cause less bronchospasm than non-selective β-blockers. Unfortunately, there is still some reluctance to the use of β-blockers in patients with COPD associated with HF, which should be eliminated.

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Floria, Mariana, Alexandru Florinel Oancea, Paula Cristina Morariu, Alexandru Burlacu, Diana Elena Iov, Cristina Petronela Chiriac, Genoveva Livia Baroi та ін. "An Overview of the Pharmacokinetics and Pharmacodynamics of Landiolol (an Ultra-Short Acting β1 Selective Antagonist) in Atrial Fibrillation". Pharmaceutics 16, № 4 (8 квітня 2024): 517. http://dx.doi.org/10.3390/pharmaceutics16040517.

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Landiolol is an ultra-short-acting, selective β1-adrenergic receptor blocker that was originally approved in Japan for the treatment of intraoperative tachyarrhythmias. It has gained attention for its use in the management of tachyarrhythmias and perioperative tachycardia, especially atrial fibrillation for both cardiac and non-cardiac surgeries. It can be the ideal agent for heart rate control due to its high β1-selectivity, potent negative chronotropic effect, a limited negative inotropic potential, and an ultrashort elimination half-life (around 4 min); moreover, it may have a potential therapeutic effects for sepsis and pediatric patients. Landiolol seems to be superior to other short-acting and selective beta-blockers such as esmolol. This review aims to provide a comprehensive overview of landiolol, a new ultra-short-acting β1 selective antagonist, including its pharmacology, clinical applications, efficacy, safety profile, and future directions in research and clinical data.

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Schnabel, Petra, Christoph Maack, Florian Mies, Stephan Tyroller, Alexander Scheer та Michael Böhm. "Binding Properties of β-Blockers at Recombinant β1-, β2-, and β3-Adrenoceptors". Journal of Cardiovascular Pharmacology 36, № 4 (жовтень 2000): 466–71. http://dx.doi.org/10.1097/00005344-200010000-00008.

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Mizogami, Maki, Ko Takakura та Hironori Tsuchiya. "The interactivities with lipid membranes differentially characterize selective and nonselective β1-blockers". European Journal of Anaesthesiology 27, № 9 (вересень 2010): 829–34. http://dx.doi.org/10.1097/eja.0b013e32833bf5e4.

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30

&NA;. "The interactivities with lipid membranes differentially characterize selective and nonselective β1-blockers". European Journal of Anaesthesiology 29, № 5 (травень 2012): 255. http://dx.doi.org/10.1097/eja.0b013e328353b02b.

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Brizzi, Vittorio, Marco Francioli, Mario Brufani, Luigi Filocamo, Giancarlo Bruni та Paola Massarelli. "Synthesis, binding affinity and selectivity of new β1- and β2-adrenoceptor blockers". Il Farmaco 54, № 11-12 (листопад 1999): 713–20. http://dx.doi.org/10.1016/s0014-827x(99)00077-4.

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32

Rizos, Ioannis K., James N. Tsoporis, Ioannis K. Toumpoulis, Vasileios Salpeas, Shehla Izhar, Angelos G. Rigopoulos, Eleftherios A. Sakadakis та Thomas G. Parker. "Antiapoptotic Effect of β1 Blockers in Ascending Thoracic Aortic Smooth Muscle Cells". Journal of Cardiovascular Pharmacology 72, № 2 (серпень 2018): 86–96. http://dx.doi.org/10.1097/fjc.0000000000000596.

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Chaudhari, Sarika, Weizu Li, Yanxia Wang, Hui Jiang, Yuhong Ma, Mark E. Davis, Jonathan E. Zuckerman та Rong Ma. "Store-operated calcium entry suppressed the TGF-β1/Smad3 signaling pathway in glomerular mesangial cells". American Journal of Physiology-Renal Physiology 313, № 3 (1 вересня 2017): F729—F739. http://dx.doi.org/10.1152/ajprenal.00483.2016.

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Our previous study demonstrated that the abundance of extracellular matrix proteins was suppressed by store-operated Ca2+entry (SOCE) in mesangial cells (MCs). The present study was conducted to investigate the underlying mechanism focused on the transforming growth factor-β1 (TGF-β1)/Smad3 pathway, a critical pathway for ECM expansion in diabetic kidneys. We hypothesized that SOCE suppressed ECM protein expression by inhibiting this pathway in MCs. In cultured human MCs, we observed that TGF-β1 (5 ng/ml for 15 h) significantly increased Smad3 phosphorylation, as evaluated by immunoblot. However, this response was markedly inhibited by thapsigargin (1 µM), a classical activator of store-operated Ca2+channels. Consistently, both immunocytochemistry and immunoblot showed that TGF-β1 significantly increased nuclear translocation of Smad3, which was prevented by pretreatment with thapsigargin. Importantly, the thapsigargin effect was reversed by lanthanum (La3+; 5 µM) and GSK-7975A (10 µM), both of which are selective blockers of store-operated Ca2+channels. Furthermore, knockdown of Orai1, the pore-forming subunit of the store-operated Ca2+channels, significantly augmented TGF-β1-induced Smad3 phosphorylation. Overexpression of Orai1 augmented the inhibitory effect of thapsigargin on TGF-β1-induced phosphorylation of Smad3. In agreement with the data from cultured MCs, in vivo knockdown of Orai1 specific to MCs using a targeted nanoparticle small interfering RNA delivery system resulted in a marked increase in abundance of phosphorylated Smad3 and in nuclear translocation of Smad3 in the glomerulus of mice. Taken together, our results indicate that SOCE in MCs negatively regulates the TGF-β1/Smad3 signaling pathway.

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Kähönen, Mika, Ritva Ylitalo, Tiit Kööbi, Väinö Turjanmaa та Pauli Ylitalo. "Influences of nonselective, β1-selective and vasodilatory β1-selective β-blockers on arterial pulse wave velocity in normotensive subjects". General Pharmacology: The Vascular System 35, № 4 (жовтень 2000): 219–24. http://dx.doi.org/10.1016/s0306-3623(01)00109-4.

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Miaron, J. O. O., та R. J. Christopherson. "Metabolic responses of the whole body, portal-drained viscera and hindquarter to adrenaline infusion: Effects of nonselective and selective β-adrenoceptor blockade". Canadian Journal of Animal Science 77, № 2 (1 червня 1997): 307–16. http://dx.doi.org/10.4141/a94-082.

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Propranolol, a nonselective β-blocker and selective β-blockers (metoprolol a β1-blocker and ICI 118551 a β2-blocker) were used to investigate the β-adrenoceptor-mediated adrenaline-induced increase in whole-body and organ VO2 in five whether sheep. Transit time blood flow probes were chronically implanted on the portal vein and the external iliac artery and sampling catheters were placed in the mesenteric artery, iliac vein and portal vein. Oxygen consumption by the whole body was measured by open circuit calorimetry, and oxygen consumption by the portal-drained viscera and the hindquarter was determined from A-VO2 differences and organ blood flow. Absolute pre-infusion VO2 values for the whole body, portal-drained viscera and hindquarters were 236 ± 7.4, 61 ± 6.0 and 13 ± 3.1 mL min−1 respectively. The mean changes in VO2 in response to infusion were 74 vs. 11, 26, 10 and 12 mL min−1 (SE = 9.1) for whole body; 31 vs. −2, −15, 13 and −4 mL min−1 (SE = 7.3) for portal-drained viscera and 8 vs. −0.4, 2.1, 1.0 and −2.7 mL min−1; SE = 4.3) for hindquarters during adrenaline, control, propranolol, metoprolol and ICI 118551 treatments, respectively. Adrenaline increased VO2 (P < 0.05) in the whole body and portal-drained viscera, but not hindquarters relative to controls. All β-blockers suppressed (P < 0.05) the adrenaline-induced increase in VO2 except for the portal-drained viscera where metoprolol was less effective and the hindquarters where β-blockers had no effect. The blood flow pattern was similar to VO2 responses for the portal-drained viscera. The nonselective β1 and β2 blockers were effective in reducing the adrenaline-induced increases in blood flow from the portal-drained viscera and to the hindquarters, with more pronounced β-adrenoceptor-mediated haemodynamic effects. The results indicate that the β-adrenoceptor system modulates whole body VO2, clearly establishes that adrenaline induces an increased VO2 in portal-drained viscera which can be reversed by a β2 or nonselective β blocker and implicates β adrenoceptors as an influencing factor in the maintenance energy requirements of ruminants. Key words: Calorimetry, adrenaline, β blockers, blood flow, sheep

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Zhang, Y. Clare, Leping Shen та M. Ian Phillips. "An Antisense β1-Reducer: Repeated Administration Reduces Hypertension and Cardiac Hypertrophy Persistently Without Toxicity or Immune Response". Hypertension 36, suppl_1 (жовтень 2000): 691. http://dx.doi.org/10.1161/hyp.36.suppl_1.691.

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72 In order to overcome the adverse effects associated with conventional β-blockers in treating hypertension, we have developed a novel β1-reducer by specifically targeting β1-adrenoceptor mRNA with an antisense oligonucleotide (β1-AS-ODN). A single intravenous injection of β1-AS-ODN deliverd with cationic liposomes caused a profound (25-35 mmHg) and prolonged (20-30 days) reduction in blood pressure in spontaneously hypertensive rats (SHR) without central effects. To be clinically useful the β1-AS-ODN would have to be effective with repeated injections and non-toxic. In this study, we have examined the effects of repeated administration of β1-AS-ODN on blood pressure and cardiac hypertrophy. Toxicity and immune response were assessed. Injections of 1mg/kg β1-AS-ODN (n=9) i.v. at 15, 20 and 26 days maintained systolic blood pressure of SHR at 20-30 mmHg lower than controls for more than 2 months (P<0.05). There was no loss in the antihypertensive efficacy with repeated injections. Instead, the intensity and duration of blood pressure reduction were greater with the second and third treatments. Control animals treated with control inverted-ODN (n=7) or saline (n=7) had no change in blood pressure with repeated injections. Left ventricular hypertrophy normalized by body weight was significantly attenuated 2 months after β1-AS-ODN treatment (P<0.05). Analysis of serum following each antisense delivery revealed no abnormalities in liver transaminase levels (ALT, AST) or hematology parameters (WBC, platelets, hematocrit). No antibodies to ODN/liposome complex were detected in gel immunodiffusion assay. Histological examination of heart, liver, kidney and spleen revealed no immunopathology or organ damage. These results demonstrate that β1-AS-ODN i.v. can be given repeatedly to achieve a sustained reduction of hypertension and reduces cardiac hypertrophy without causing toxic effects or immune stimulation. These data, together with results of our previous studies, show β1-AS-ODN is viable as a potentially new prolonged antihypertensive agent with benefits on cardiac remodeling.

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Ongali, Brice, Nektaria Nicolakakis, Xin-Kang Tong, Clotilde Lecrux, Hans Imboden та Edith Hamel. "Transforming growth factor-β1 induces cerebrovascular dysfunction and astrogliosis through angiotensin II type 1 receptor-mediated signaling pathways". Canadian Journal of Physiology and Pharmacology 96, № 5 (травень 2018): 527–34. http://dx.doi.org/10.1139/cjpp-2017-0640.

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Transgenic mice constitutively overexpressing the cytokine transforming growth factor-β1 (TGF-β1) (TGF mice) display cerebrovascular alterations as seen in Alzheimer’s disease (AD) and vascular cognitive impairment and dementia (VCID), but no or only subtle cognitive deficits. TGF-β1 may exert part of its deleterious effects through interactions with angiotensin II (AngII) type 1 receptor (AT1R) signaling pathways. We test such interactions in the brain and cerebral vessels of TGF mice by measuring cerebrovascular reactivity, levels of protein markers of vascular fibrosis, nitric oxide synthase activity, astrogliosis, and mnemonic performance in mice treated (6 months) with the AT1R blocker losartan (10 mg/kg per day) or the angiotensin converting enzyme inhibitor enalapril (3 mg/kg per day). Both treatments restored the severely impaired cerebrovascular reactivity to acetylcholine, calcitonin gene-related peptide, endothelin-1, and the baseline availability of nitric oxide in aged TGF mice. Losartan, but not enalapril, significantly reduced astrogliosis and cerebrovascular levels of profibrotic protein connective tissue growth factor while raising levels of antifibrotic enzyme matrix metallopeptidase-9. Memory was unaffected by aging and treatments. The results suggest a pivotal role for AngII in TGF-β1-induced cerebrovascular dysfunction and neuroinflammation through AT1R-mediated mechanisms. Further, they suggest that AngII blockers could be appropriate against vasculopathies and astrogliosis associated with AD and VCID.

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Park, Soo Hyun, and Ho Jae Han. "The mechanism of angiotensin II binding downregulation by high glucose in primary renal proximal tubule cells." American Journal of Physiology-Renal Physiology 282, no. 2 (February 1, 2002): F228—F237. http://dx.doi.org/10.1152/ajprenal.00080.2001.

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The renin-angiotensin system plays an important role in the development of diabetic nephropathy. However, the mechanism of ANG II receptor regulation in the renal proximal tubule in the diabetic condition has not been elucidated. Thus we investigated the signal pathways involved in high-glucose-induced downregulation of ANG II binding in primary cultured renal proximal tubule cells. Twenty-five millimolar glucose, but not mannitol andl-glucose, induced downregulation of the AT1receptor (AT1R) because of a significant decline in maximal binding with no significant change in the affinity constant. Twenty-five millimolar glucose also decreased AT1R mRNA and protein levels. The 25 mM glucose-induced increase in the formation of lipid peroxides was prevented by antioxidants, protein kinase C (PKC) inhibitors, or L-type calcium channel blockers. These agents also blocked 25 mM glucose-induced downregulation of 125I-ANG II binding. In addition, 25 mM glucose increased transforming growth factor (TGF)-β1 secretion, and anti-TGF-β antibody significantly blocked 25 mM glucose-induced downregulation of 125I-ANG II binding. Furthermore, the 25 mM glucose-induced increase in TGF-β1 secretion was inhibited by PKC inhibitors, L-type calcium channel blockers, or antioxidants. In conclusion, high glucose may induce downregulation of 125I-ANG II binding via a PKC-oxidative stress-TGF-β signal cascade in primary cultured rabbit renal proximal tubule cells.

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Ozakca, Isil, Ebru Arioglu-Inan, Hrag Esfahani, V. Melih Altan, Jean-Luc Balligand, Gizem Kayki-Mutlu та A. Tanju Ozcelikay. "Nebivolol prevents desensitization of β-adrenoceptor signaling and induction of cardiac hypertrophy in response to isoprenaline beyond β1-adrenoceptor blockage". American Journal of Physiology-Heart and Circulatory Physiology 304, № 9 (1 травня 2013): H1267—H1276. http://dx.doi.org/10.1152/ajpheart.00352.2012.

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The importance of chronic stimulation of β-adrenoceptors in the development of cardiac dysfunction is the rationale for the use of β-blockers in the treatment of heart failure. Nebivolol is a third-generation β-blocker, which has further properties including stimulation of endothelial nitric oxide synthase and/or β3-adrenoceptors. The aim of this study was to investigate whether nebivolol has additional effects on β-adrenoceptor-mediated functional responses along with morphologic and molecular determinants of cardiac hypertrophy compared with those of metoprolol, a selective β1-adrenoceptor blocker. Rats infused by isoprenaline (100 μg·kg−1·day−1, 14 days) were randomized into three groups according to the treatment with metoprolol (30 mg·kg−1·day−1), nebivolol (10 mg·kg−1·day−1), or placebo for 13 days starting on day 1 after implantation of minipump. Both metoprolol and nebivolol caused a similar reduction on heart rate. Nebivolol mediated a significant improvement on cardiac mass, coronary flow, mRNA expression levels of sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) and atrial natriuretic peptide and phospholamban (PLN)/SERCA2a and phospho-PLN/PLN ratio compared with metoprolol and placebo. Nebivolol prevented the detrimental effects of isoprenaline infusion on isoprenaline (68% of control at 30 μM), BRL37344 (63% of control at 0.1 μM), and forskolin (64% of control at 1 μM) responses compared with metoprolol (isoprenaline, 34% of control; BRL37344, no response; forskolin, 26% of control) and placebo (isoprenaline, 33% of control; BRL37344, 28% of control; forskolin, 12% of control). Both β-blockers improved the changes in mRNA expressions of β1- and β3-adrenoceptors. Our results suggest that nebivolol partially protects the responsiveness of β-adrenoceptor signaling and the development of cardiac hypertrophy independent of its β1-adrenoceptor blocking effect.

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Kruik-Kollöffel, Willemien J., Job van der Palen, Carine J. M. Doggen, Marissa C. van Maaren, H. Joost Kruik, Edith M. Heintjes, Kris L. L. Movig, and Gerard C. M. Linssen. "Heart failure medication after a first hospital admission and risk of heart failure readmission, focus on beta-blockers and renin-angiotensin-aldosterone system medication: A retrospective cohort study in linked databases." PLOS ONE 15, no. 12 (December 22, 2020): e0244231. http://dx.doi.org/10.1371/journal.pone.0244231.

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Background This study assessed the association between heart failure (HF) medication (angiotensin-converting-enzyme inhibitors (ACEI)/angiotensin-receptor blockers (ARB), beta-blockers (BB), mineralocorticoid-receptor antagonists (MRA) and diuretics) and HF readmissions in a real-world unselected group of patients after a first hospital admission for HF. Furthermore we analysed readmission rates for ACEI versus ARB and for carvedilol versus β1-selective BB and we investigated the effect of HF medication in relation to time since discharge. Methods and findings Medication at discharge was determined with dispensing data from the Dutch PHARMO Database Network including 22,476 patients with HF between 2001 and 2015. After adjustment for age, gender, number of medications and year of admission no associations were found for users versus non-users of ACEI/ARB (hazard ratio, HR = 1.01; 95%CI 0.96–1.06), BB (HR = 1.00; 95%CI 0.95–1.05) and readmissions. The risk of readmission for patients prescribed MRA (HR = 1.11; 95%CI 1.05–1.16) or diuretics (HR = 1.17; 95%CI 1.09–1.25) was higher than for non-users. The HR for ARB relative to ACEI was 1.04 (95%CI 0.97–1.12) and for carvedilol relative to β1-selective BB 1.33 (95%CI 1.20–1.46). Post-hoc analyses showed a protective effect shortly after discharge for most medications. For example one month post discharge the HR for ACEI/ARB was 0.77 (95%CI 0.69–0.86). Although we did try to adjust for confounding by indication, probably residual confounding is still present. Conclusions Patients who were prescribed carvedilol have a higher or at least a similar risk of HF readmission compared to β1-selective BB. This study showed that all groups of HF medication -some more pronounced than others- were more effective immediately following discharge.

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Gutierrez, Guillermo, та Guillermo Ballarino. "Gut mucosal permeability, β1 receptor blockers and gastric tonometry: the time is now!" Intensive Care Medicine 37, № 11 (17 серпня 2011): 1721–22. http://dx.doi.org/10.1007/s00134-011-2330-1.

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Nemoto, Shinji, Yusuke Kasahara, Kazuhiro P. Izawa, Satoshi Watanabe, Kazuya Yoshizawa, Naoya Takeichi, Kentaro Kamiya та ін. "Effects of αβ-Blocker Versus β1-Blocker Treatment on Heart Rate Response During Incremental Cardiopulmonary Exercise in Japanese Male Patients with Subacute Myocardial Infarction". International Journal of Environmental Research and Public Health 16, № 16 (8 серпня 2019): 2838. http://dx.doi.org/10.3390/ijerph16162838.

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A simplified substitute for heart rate (HR) at the anaerobic threshold (AT), i.e., resting HR plus 30 beats per minute or a percentage of predicted maximum HR, is used as a way to determine exercise intensity without cardiopulmonary exercise testing (CPX) data. However, difficulties arise when using this method in subacute myocardial infarction (MI) patients undergoing beta-blocker therapy. This study compared the effects of αβ-blocker and β1-blocker treatment to clarify how different beta blockers affect HR response during incremental exercise. MI patients were divided into αβ-blocker (n = 67), β1-blocker (n = 17), and no-β-blocker (n = 47) groups. All patients underwent CPX one month after MI onset. The metabolic chronotropic relationship (MCR) was calculated as an indicator of HR response from the ratio of estimated HR to measured HR at AT (MCR-AT) and peak exercise (MCR-peak). MCR-AT and MCR-peak were significantly higher in the αβ-blocker group than in the β1-blocker group (p < 0.001, respectively). Multiple regression analysis revealed that β1-blocker but not αβ-blocker treatment significantly predicted lower MCR-AT and MCR-peak (β = −0.432, p < 0.001; β = −0.473, p < 0.001, respectively). Based on these results, when using the simplified method, exercise intensity should be prescribed according to the type of beta blocker used.

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Brahmbhatt, Shruti Vihang, and Bhagya M. Sattigeri. "A study on management of hypertension in patients with type 2 diabetes mellitus in tertiary care teaching rural hospital." International Journal of Basic & Clinical Pharmacology 7, no. 11 (October 23, 2018): 2196. http://dx.doi.org/10.18203/2319-2003.ijbcp20184327.

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Background: This study was aimed to analyze the drug utilization pattern in the management of hypertension in diabetic patients.Methods: A prospective, observational and non interventional study was conducted in 100 diabetic hypertensive patients admitted in medicine wards at Dhiraj Hospital. Patients who signed informed consent form were only included in the study. All the data were recorded from patients’ case files and analyzed.Results: Of enrolled 100 patients, 69 (69%) were male and 31 (31%) were female and maximum number of the patients (42%) were found in the age group of 51-60 years. Out of 100 admitted patients, 75% patients were treated with single antihypertensive agent, 20% were treated with combination of two antihypertensive agents while only 5% were administered more than two antihypertensive agents. As a single antihypertensive agent, most commonly prescribed was ACE inhibitors (32%), Calcium Channel Blockers (23%), Angiotensin Receptor Blockers (12%) and β1 blockers (8%).Conclusions: There was poor awareness among the patients regarding control of hypertension, regular follow up, medication adherence etc. However, two third of diabetic patients had achieved blood pressure target control and ACE inhibitor remained first choice of drug for hypertension in diabetes in this study.

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Pillozzi, Serena, Marika Masselli, Emanuele De Lorenzo, Benedetta Accordi, Emanuele Cilia, Olivia Crociani, Amedeo Amedei, et al. "Chemotherapy resistance in acute lymphoblastic leukemia requires hERG1 channels and is overcome by hERG1 blockers." Blood 117, no. 3 (January 20, 2011): 902–14. http://dx.doi.org/10.1182/blood-2010-01-262691.

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Abstract Bone marrow mesenchymal cells (MSCs) can protect leukemic cells from chemotherapy, thus increasing their survival rate. We studied the potential molecular mechanisms underlying this effect in acute lymphoblastic leukemia (ALL) cells. Coculture of ALL cells with MSCs induced on the lymphoblast plasma membrane the expression of a signaling complex formed by hERG1 (human ether-à-go-go-related gene 1) channels, the β1-integrin subunit, and the chemokine receptor CXC chemokine receptor-4. The assembly of such a protein complex activated both the extracellular signal-related kinase 1/2 (ERK1/2) and the phosphoinositide 3-kinase (PI3K)/Akt prosurvival signaling pathways. At the same time, ALL cells became markedly resistant to chemotherapy-induced apoptosis. hERG1 channel function appeared to be important for both the initiation of prosurvival signals and the development of drug resistance, because specific channel blockers decreased the protective effect of MSCs. NOD/SCID mice engrafted with ALL cells and treated with channel blockers showed reduced leukemic infiltration and had higher survival rates. Moreover, hERG1 blockade enhanced the therapeutic effect produced by corticosteroids. Our findings provide a rationale for clinical testing of hERG1 blockers in the context of antileukemic therapy for patients with ALL.

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Polakovičová, M., та R. Čižmáriková. "Molecular Docking Study on the Binding Mode of Cardioselective Phenoxyaminopropanol Blocker into β-adrenergic Receptor Subtypes". Acta Facultatis Pharmaceuticae Universitatis Comenianae 59, № 2 (28 грудня 2012): 44–53. http://dx.doi.org/10.2478/v10219-012-0024-6.

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AbstractStructural understanding of subtype specific ligand-binding pocket variations and interactions of ligand with receptor may facilitate design of novel selective drugs. To gain insights into the subtype selectivity of β-blockers we performed flexible molecular docking study to analyze the interaction mode of cardioselective phenoxyaminopropanol blocker into the β1 and β2-adrenergic receptor. The binding site analysis reveals a strong identity between important amino acid residues and interactions with ligand in orthosteric catecholamine- binding pocket. The differences in the binding mode of selective ligand have been identified in the extracellular region of receptor subtypes.

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Ahmed, Maruf, Habib Abul Muntasir, Murad Hossain, Masaji Ishiguro, Tadazumi Komiyama, Ikunobu Muramatsu, Hitoshi Kurose та Takafumi Nagatomo. "Beta-Blockers Show Inverse Agonism to a Novel Constitutively Active Mutant of β1-Adrenoceptor". Journal of Pharmacological Sciences 102, № 2 (2006): 167–72. http://dx.doi.org/10.1254/jphs.fp0060640.

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Song, Hong Ji, Joongyub Lee, Ye-Jee Kim, Sun-Young Jung, Hwa Jung Kim, Nam-Kyong Choi та Byung-Joo Park. "β1 selectivity of β-blockers and reduced risk of fractures in elderly hypertension patients". Bone 51, № 6 (грудень 2012): 1008–15. http://dx.doi.org/10.1016/j.bone.2012.08.126.

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Brizzi, Vittorio, Marco Francioli, Mario Brufani, Luigi Filocamo, Giancarlo Bruni та Paola Massarelli. "ChemInform Abstract: Synthesis, Binding Affinity, and Selectivity of New β1- and β2-Adrenoceptor Blockers." ChemInform 31, № 12 (9 червня 2010): no. http://dx.doi.org/10.1002/chin.200012248.

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Jia, Haiyan, Sue Monteith та Morris J. Brown. "Expression of the α- and β-Subunits of the Stimulatory and Inhibitory G-Proteins in β1-Adrenoceptor-Blocked and non-β-Adrenoceptor-Blocked Human Atrium". Clinical Science 88, № 5 (1 травня 1995): 571–80. http://dx.doi.org/10.1042/cs0880571.

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1. Chronic β1-adrenoceptor blocker therapy induces hyperresponsiveness of the β2-adrenoceptor in human atrium. To investigate whether the β2-adrenoceptor sensitization induced by β1-adrenoceptor blockade is associated with altered gene expression of G-proteins, which couple the receptors to adenylate cyclase, we determined the mRNA expression of the α- and β-subunits of the stimulatory G-protein, Gs, and inhibitory G-protein, Gi, in human right atrial appendage by polymerase chain reaction and by enhanced chemiluminescence Northern blot analysis. 2. The polymerase chain reaction revealed bands of predicted size of Gsα, both short form and long form, all three Giα subtypes and three Gβ subtypes. In Northern blots, the digoxigenin-labelled antisense cRNA probe specific for Giα2 hybridized to a predominant band at 2.3 kb, whereas the Giα3 cRNA probe detected a message of 1.8 kb in total RNA extracted from human atrium. The cRNA probe encoding Gsα revealed one major band at 1.9 kb and one minor band at 1.7 kb. The Gβ cRNA probes detected messages of 3.4 kb for Gβ1, 1.8 kb for Gβ2 and 1.9 kb for Gβ3 in human atrium. 3. The mRNA levels of Gsα in β1-adrenoceptor-blocked atria (n = 12) were not significantly different from those in non-β-adrenoceptor-blocked atria (n = 12), nor were there any significant differences in the Giα2 mRNA levels between atria from patients treated with β1-adrenoceptor blockers and untreated patients. The ratios of 1.9-kb Gsα mRNA to 1.7-kb Gsα mRNA and of 1.9-kb Gsα mRNA to 2.3-kb Giα2 mRNA in β1-adrenoceptor-blocked patients were almost identical to those in non-β-adrenoceptor-blocked patients. Neither Gβ1 mRNA nor Gβ2 mRNA expression in β1-adrenoceptor-blocked atria differed significantly from that in non-β-adrenoceptor-blocked atria. 4. We conclude that the previously observed sensitization following β1-adrenoceptor-blockade of β2-adrenoceptors in human atria is unlikely to be mediated by altered gene expression of the α- and β-subunits of G-proteins.

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Gao, Xiaomeng, Jingyue Chang, Yi Chang, Lili Fan, Ziqian Liu, Cuijuan Zhang, Tatsuo Shimosawa, Fan Yang та Qingyou Xu. "Esaxerenone Inhibits Renal Angiogenesis and Endothelial-Mesenchymal Transition via the VEGFA and TGF-β1 Pathways in Aldosterone-Infused Mice". International Journal of Molecular Sciences 24, № 14 (21 липня 2023): 11766. http://dx.doi.org/10.3390/ijms241411766.

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Renal fibrosis is an inevitable process in the progression of chronic kidney disease (CKD). Angiogenesis plays an important role in this process. Vascular endothelial cells are involved in renal fibrosis by phenotypic transformation and secretion of extracellular matrix. Aldosterone stimulates mineralocorticoid receptor (MR) activation and induces inflammation, which is important for angiogenesis. Clinically, MR blockers (MRBs) have a protective effect on damaged kidneys, which may be associated with inhibition of angiogenesis. In this study, we used aldosterone-infused mice and found that aldosterone induced angiogenesis and that endothelial-mesenchymal transition (EndMT) in neovascular endothelial cells was involved in renal fibrosis. Notably, aldosterone induced inflammation and stimulated macrophages to secrete vascular endothelial growth factor (VEGF) A to regulate angiogenesis by activating MR, whereas EndMT occurred in response to transforming growth factor-β1 (TGF-β1) induction and participated in renal fibrosis. These effects were antagonized by the MRB esaxerenone. These findings suggest that reducing angiogenesis may be an effective strategy for treating renal fibrosis.

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