(S)-(-)-Atenolol is a potent β-adrenergic receptor blocker[1]. (S)-(-)-Atenolol is the S(-) enantiomer of Atenolol, while the R(+) enantiomer of Atenolol has almost no β-receptor blocker activity[2, 3]. (S)-(-)-Atenolol is mainly used to treat hypertension and heart-related chest pain[4].
In vitro, (S)-(-)-Atenolol (0-350μM) treated vascular smooth muscle A7r5 cells for 24h inhibited cell viability in a dose-dependent manner and reduced the levels of calmodulin and annexin A6 in the cells[5]. (S)-(-)-Atenolol (200, 400, 600μM) treated MCF7 cells for 72h significantly inhibited cell migration and reduced the percentage of wound healing (WH) of the cells[6].
In vivo, (S)-(-)-Atenolol (90mg/kg/day) was orally administered to spontaneously hypertensive rats for 8 weeks and was less effective in reducing carotid systolic blood pressure than Carvedilol (30mg/kg/day) or Nebivolol (30mg/kg/day)[7].
References:
[1] Mehvar R, Brocks D R. Stereospecific pharmacokinetics and pharmacodynamics of beta-adrenergic blockers in humans[J]. 2001.
[2] Seebauer C T, Graus M S, Huang L, et al. Non–beta blocker enantiomers of propranolol and atenolol inhibit vasculogenesis in infantile hemangioma[J]. The Journal of Clinical Investigation, 2022, 132(3).
[3] Stoschitzky K, Egginger G, Zernig G, et al. Stereoselective features of (R)‐and (S)‐atenolol: Clinical pharmacological, pharmacokinetic, and radioligand binding studies[J]. Chirality, 1993, 5(1): 15-19.
[4] Heel R C, Brogden R N, Speight T M, et al. Atenolol: a review of its pharmacological properties and therapeutic efficacy in angina pectoris and hypertension[J]. Drugs, 1979, 17: 425-460.
[5] Sui J, Zhang J, Tan T L, et al. Comparative proteomics analysis of vascular smooth muscle cells incubated with S-and R-enantiomers of atenolol using iTRAQ-coupled two-dimensional LC-MS/MS[J]. Molecular & Cellular Proteomics, 2008, 7(6): 1007-1018.
[6] İşeri Ö D, Sahin F I, Terzi Y K, et al. beta-Adrenoreceptor antagonists reduce cancer cell proliferation, invasion, and migration[J]. Pharmaceutical biology, 2014, 52(11): 1374-1381.
[7] Del Mauro J S, Prince P D, Allo M A, et al. Effects of third-generation β-blockers, atenolol or amlodipine on blood pressure variability and target organ damage in spontaneously hypertensive rats[J]. Journal of Hypertension, 2020, 38(3): 536-545.
(S)-(-)-Atenolol是一种强效的β-肾上腺素能受体阻滞剂[1]。(S)-(-)-Atenolol是Atenolol的S(-)对映体，Atenolol的R(+)对映体几乎不具有β受体阻滞剂活性[2, 3]。(S)-(-)-Atenolol主要用于治疗高血压和与心脏相关的胸痛[4]。
在体外，(S)-(-)-Atenolol（0-350μM）处理血管平滑肌A7r5细胞24h，以剂量依赖性方式抑制了细胞活力，降低了细胞中钙调蛋白和膜联蛋白A6的水平[5]。(S)-(-)-Atenolol（200, 400, 600μM）处理MCF7细胞72h，显著抑制了细胞迁移，降低了细胞的伤口愈合百分比（WH）[6]。
在体内，(S)-(-)-Atenolol（90mg/kg/day）通过口服治疗自发性高血压大鼠8周，降低颈动脉收缩压的疗效较低，效果不如卡维地洛（Carvedilol，30mg/kg/day）或奈必洛尔（Nebivolol，30mg/kg/day）[7]。