Israel A, Sosa-Canache B
School of Pharmacy, Universidad Central de Venezuela, Caracas, Venezuela.
J Hum Hypertens. 2002 Mar;16 Suppl 1:S84-8. doi: 10.1038/sj.jhh.1001350.
The present study was carried out to assess whether endogenous angiotensin II (Ang II) supports sympathetically mediated cardiovascular response to stress in conscious unrestrained rats, using experimental models in which the renin-angiotensin-system was reduced or blocked. Footshock-stress increased mean arterial pressure (MAP) and heart rate (HR). Inhibition of angiotensin-converting enzyme with captopril or blockade of AT(1)angiotensin receptor with losartan, attenuated vasopressor responses to footshocks, while heart rate response was not altered. Bilateral nephrectomy suppressed vasopressor response as well the elevation of plasma noradrenaline and adrenaline induced by footshocks, and reduced heart rate response. Cardiovascular response to stress in nephrectomised rats was restored by exogenous administration of a subpressor dose of Ang II. Our results demonstrate that in conscious rats cardiovascular response to footshocks is dependent on an active renin-angiotensin system and they indicate that endogenous Ang II supports the sympathetically mediated vasopressor response to footshocks.
本研究旨在利用降低或阻断肾素 - 血管紧张素系统的实验模型,评估内源性血管紧张素II(Ang II)是否支持清醒自由活动大鼠对压力的交感神经介导的心血管反应。足底电击应激增加了平均动脉压(MAP)和心率(HR)。用卡托普利抑制血管紧张素转换酶或用氯沙坦阻断AT(1)血管紧张素受体,减弱了对足底电击的升压反应,而心率反应未改变。双侧肾切除抑制了升压反应以及足底电击诱导的血浆去甲肾上腺素和肾上腺素升高,并降低了心率反应。通过外源性给予亚升压剂量的Ang II可恢复肾切除大鼠对压力的心血管反应。我们的结果表明,在清醒大鼠中,对足底电击的心血管反应依赖于活跃的肾素 - 血管紧张素系统,并且表明内源性Ang II支持对足底电击的交感神经介导的升压反应。