Angiotensin II (ANG II) is part of the renin-angiotensin system (RAS) in vertebrates and exert vasoconstriction in all species studied. The present study examines the vasopressor effect of ANG II in the ball python (Python regius), and examines whether ANG II exert its effect through direct angiotensin receptors or through an activation of α-adrenergic receptors. The studies were conducted in snakes with chronic arterial catheters that had recovered from anesthesia. In addition to demonstrating a clear and pronounced dose-dependent rise in arterial blood pressure upon repeated injections of boluses with ANG II (0.001–1 μg/kg), we demonstrate that the pressor response persisted following α-adrenergic blockade using the α-adrenergic antagonist phentolamine (2.5 mg/kg). Unfortunately, it proved impossible to block the ANG receptors using losartan (1, 3 or even 10 mg/kg). The pressor response to ANG II was associated with a significant rise in heart rate at the higher dosages, pointing to a resetting of the barostatic mechanism for heart rate regulation. The responses were similar in fasting and digesting pythons despite the expected rise in baseline values for blood pressure and heart rate of the digesting snakes.

血管紧张素II（ANG II）是脊椎动物的肾素-血管紧张素系统（RAS）的一部分，在所有研究的物种中均发挥血管收缩作用。本研究考察了ANG II在球形蟒蛇（Python regius）中的血管升压作用。），并检查ANG II是否通过直接的血管紧张素受体或通过激活α-肾上腺素受体发挥作用。该研究是在从麻醉中恢复过来的带有慢性动脉导管的蛇中进行的。除了证明在重复注射ANG II（0.001–1μg/ kg）团注后，动脉血压明显且明显的剂量依赖性升高外，我们还证明了在使用α-肾上腺素进行α-肾上腺素阻断后，升压反应持续存在拮抗剂酚妥拉明（2.5 mg / kg）。不幸的是，事实证明使用氯沙坦（1、3甚至10 mg / kg）无法阻断ANG受体。在较高剂量下，对ANG II的升压反应与心率显着升高有关，这表明用于心率调节的静压机制的复位。