Metoprolol is a selective β1 receptor blocker [1]. Metoprolol slows down the heart rate, reduces myocardial contractility and cardiac output by inhibiting β1-adrenergic receptors in the heart, thereby reducing myocardial oxygen consumption and stabilizing heart rhythm [2]. Metoprolol is commonly used to treat hypertension, angina pectoris, arrhythmia and other diseases [3-4].
In human retinal endothelial cells (HREC), Metoprolol (1µM, 10µM; 24h, 48h) counteracts the increase in the tube-like structures of HREC stimulated with high glucose [5]. In rat cardiac myocytes, Metoprolol (3µM; 12h) but not carvedilol prevents isoprenaline-induced downregulation of myocyte b-adrenoceptors [6]. In neutrophils, Metoprolol (0.3-300µM; 40min) dose-dependently inhibits neutrophil migration induced by formyl peptide [7].
In isoflurane anesthetized mice models, Metoprolol (3mg/kg; iv; single injection) caused a reduction in HR, SV, and CO, while SVR increased [8]. In ApoE-/- mice, Metoprolol (2.5mg/kg; iv; 11 weeks) reduced atherosclerotic plaque area [9]. In collagenase-injection intracerebral hemorrhage (ICH) mice model Metoprolol (2.5mg/kg; ig; 14d) attenuates intracerebral hemorrhage-induced cardiac damage by suppression of sympathetic overactivity [10].
References:
[1]. Koch-Weser J. Metoprolol. New England Journal of Medicine. 1979 Sep 27; 301(13): 698-703.
[2]. Rangno RE, Langlois S, Lutterodt A. Metoprolol withdrawal phenomena: mechanism and prevention. Clinical Pharmacology & Therapeutics. 1982 Jan; 31(1): 8-15.
[3]. Merit-HF Study Group. Effect of metoprolol CR/XL in chronic heart failure: metoprolol CR/XL randomised intervention trial in-congestive heart failure (MERIT-HF). The Lancet. 1999 Jun 12;353(9169): 2001-2007.
[4]. Brogden RN, Heel RC, Speight TM, et al. Metoprolol: a review of its pharmacological properties and therapeutic efficacy in hypertension and angina pectoris. Drugs. 1977 Nov; 14: 321-348.
[5]. Giurdanella G, Longo A, Distefano A, et al. The anti-inflammatory effect of the β1-adrenergic receptor antagonist metoprolol on high glucose treated human microvascular retinal endothelial cells. Cells. 2021 Dec 24; 11(1): 51.
[6]. Flesch M, Ettelbrück S, Rosenkranz S, Maack C, Cremers B, Schlüter KD, Zolk O, Böhm M. Differential effects of carvedilol and metoprolol on isoprenaline-induced changes in β-adrenoceptor density and systolic function in rat cardiac myocytes. Cardiovascular research. 2001 Feb 1; 49(2): 371-380.
[7]. Dunzendorfer S, Wiedermann CJ. Modulation of neutrophil migration and superoxide anion release by metoprolol. Journal of molecular and cellular cardiology. 2000 Jun 1; 32(6): 915-924.
[8]. El Beheiry MH, Heximer SP, Voigtlaender-Bolz J, et al. Metoprolol impairs resistance artery function in mice. Journal of Applied Physiology. 2011 Oct; 111(4): 1125-1133.
[9]. Ulleryd MA, Bernberg E, Yang LJ, et al. Metoprolol reduces proinflammatory cytokines and atherosclerosis in ApoE−/− mice. BioMed research international. 2014; 2014(1): 548783.
[10]. Zhang L, Wuri J, An L, et al. Metoprolol attenuates intracerebral hemorrhage-induced cardiac damage by suppression of sympathetic overactivity in mice. Autonomic Neuroscience. 2021 Sep 1; 234: 102832.
Metoprolol是一种选择性β1受体阻滞剂 [1]。Metoprolol通过抑制心脏内的β1-肾上腺素受体，减慢心率，降低心肌收缩力和心输出量，从而降低心肌耗氧量，稳定心律 [2]。Metoprolol常用于治疗高血压、心绞痛、心律失常等疾病 [3-4]。
在人视网膜内皮细胞（HREC）中，Metoprolol（1µM、10µM；24h、48h）可抵消高葡萄糖刺激后HREC管状结构的增加 [5]。在大鼠心肌细胞中，Metoprolol（3µM；12h）能阻止异丙肾上腺素诱导的心肌细胞β-肾上腺素能受体下调，而卡维地洛则不能 [6]. 在中性粒细胞中，Metoprolol（0.3-300µM；40分钟）剂量依赖性地抑制甲酰肽诱导的中性粒细胞迁移 [7]。
在异氟烷麻醉小鼠模型中，Metoprolol（3mg/kg；iv；单次注射）导致HR、SV和CO降低，而SVR增加 [8]。在 ApoE-/-小鼠中，Metoprolol（2.5mg/kg；iv；11周）减少了动脉粥样硬化斑块面积 [9]。在胶原酶注射脑出血（ICH）小鼠模型中，Metoprolol（2.5mg/kg；ig；14d）通过抑制交感神经过度活跃来减轻脑出血引起的心脏损害 [10]。