在植入遥测设备的大鼠中,用阿曲生坦阻断内皮素A受体可预防多靶点酪氨酸激酶抑制剂ABT - 869所致的高血压。
ETA receptor blockade with atrasentan prevents hypertension with the multitargeted tyrosine kinase inhibitor ABT-869 in telemetry-instrumented rats.
作者信息
Banfor Patricia N, Franklin Pamela A, Segreti Jason A, Widomski Deborah L, Davidsen Steven K, Albert Daniel H, Cox Bryan F, Fryer Ryan M, Gintant Gary A
机构信息
Department of Integrative Pharmacology, Global Pharmaceutical Research and Development, Abbott Laboratories, Abbott Park, IL 60064-6119, USA.
出版信息
J Cardiovasc Pharmacol. 2009 Feb;53(2):173-8. doi: 10.1097/FJC.0b013e3181993493.
ABT-869 is a novel multitargeted inhibitor of vascular endothelial growth factor and platelet-derived growth factor receptor tyrosine kinases (RTKs) with potent antiangiogenic properties that slow tumor progression. Vascular endothelial growth factor receptor blockade has been shown to produce hypertension. Atrasentan is a potent and selective endothelin (ETA) receptor antagonist that lowers blood pressure and affects tumor growth. To assess the utility of ETA receptor blockade in controlling hypertension with RTK inhibition, we evaluated the ability of atrasentan to block hypertension with ABT-869 in conscious, telemetry-instrumented rats. Changes in mean arterial pressure (MAP) and heart rate (HR) were evaluated using mean values and the area under the curve (AUC). Atrasentan (0.5, 1.5, and 5.0 mg kg(-1) d(-1) for 5 days) elicited dose-dependent decreases in MAP-AUC (-16.7 +/- 1.3, -20.94 +/- 3.68, and -30.12 +/- 3.57 mm Hg x day, respectively) compared with vehicle. ABT-869 (1, 3, 10, 30 mg kg(-1) d(-1) for 5 days) increased MAP compared with vehicle (MAP-AUC values of -5.52 +/- 3.75, 12.7 +/- 8.4, 37.5 +/- 4.4, and 63.8 +/- 3.3 mm Hg x day, respectively). Pretreatment with atrasentan (5 mg/kg for 5 days) prevented and abolished the hypertensive effects of ABT-869. Thus, ETA receptor blockade effectively alleviated hypertension with RTK inhibition and may serve a dual therapeutic role by preventing hypertension and slowing tumor progression.
ABT - 869是一种新型的多靶点血管内皮生长因子和血小板衍生生长因子受体酪氨酸激酶(RTKs)抑制剂,具有强大的抗血管生成特性,可减缓肿瘤进展。血管内皮生长因子受体阻断已被证明会导致高血压。阿曲生坦是一种强效且选择性的内皮素(ETA)受体拮抗剂,可降低血压并影响肿瘤生长。为了评估ETA受体阻断在控制RTK抑制引起的高血压中的效用,我们在有意识的、植入遥测设备的大鼠中评估了阿曲生坦与ABT - 869联合使用时阻断高血压的能力。使用平均值和曲线下面积(AUC)评估平均动脉压(MAP)和心率(HR)的变化。与赋形剂相比,阿曲生坦(0.5、1.5和5.0 mg·kg⁻¹·d⁻¹,连续5天)引起MAP - AUC呈剂量依赖性降低(分别为-16.7±1.3、-20.94±3.68和-30.12±3.57 mmHg·天)。与赋形剂相比,ABT - 869(1、3、10、30 mg·kg⁻¹·d⁻¹,连续5天)使MAP升高(MAP - AUC值分别为-5.52±3.75、12.7±8.4、37.5±4.4和63.8±3.3 mmHg·天)。阿曲生坦预处理(5 mg/kg,连续5天)预防并消除了ABT - 869的高血压作用。因此,ETA受体阻断可有效减轻RTK抑制引起的高血压,并且通过预防高血压和减缓肿瘤进展可能发挥双重治疗作用。