Mechanisms of the central pressor action of angiotensin II in conscious rats.
Mechanisms of the central pressor action of angiotensin II in conscious rats.
复制标题
血管紧张素 II 对清醒大鼠的中枢升压作用机制。
作者：
R. Lappe;M. Brody
先前的研究已经证明，由于中枢作用，通过大鼠颈动脉输注的血管紧张素II（ANG II）比通过腹主动脉输注的ANG II引起更大的升压反应。在本研究中，区域血管阻力反应，颈动脉和腹主动脉血管紧张素II和血管紧张素I（ANG I）的输液进行了比较清醒的无约束大鼠。使用微型脉冲多普勒血流探头记录局部血流。颈动脉和主动脉输注引起后躯、肾和肠系膜血管床血管收缩;颈动脉途径导致动脉压和局部血管阻力更大幅度增加。血管紧张素II的颈动脉灌注增强血管收缩反应显着衰减全身六甲铵或中央saralasin。与ANG II不同，ANG I的颈动脉和主动脉输注产生了不受中枢saralasin影响的等效区域血管收缩反应。它的结论是，除了其周边效应，血管紧张素II的中枢作用诱导神经介导的血管收缩的后躯，肾，肠系膜血管床。ANG II的中枢效应似乎不是由血液传播的ANG I在脑中的转化引起的。
Previous studies have demonstrated that, due to a central action, angiotensin II (ANG II) infused via the carotid artery of the rat elicited a greater pressor response than ANG II infused via the abdominal aorta. In the present study, regional vascular resistance responses to carotid and abdominal aortic infusions of ANG II and angiotensin I (ANG I) were compared in conscious unrestrained rats. Miniaturized pulsed Doppler flow probes were used to record regional blood flows. Carotid and aortic infusions caused vasoconstriction in the hindquarters, renal, and mesenteric vascular beds; the carotid route resulted in greater increases in arterial pressure and regional vascular resistances. The enhanced vasoconstrictor responses to carotid infusions of ANG II were significantly attenuated by systemic hexamethonium or central saralasin. Unlike ANG II, carotid and aortic infusions of ANG I produced equivalent regional vasoconstrictor responses not affected by central saralasin. It is concluded that in addition to its peripheral effects, central actions of ANG II induce neurally mediated vasoconstriction of the hindquarters, renal, and mesenteric vascular beds. Central effects of ANG II do not appear to result from conversion in the brain of blood-borne ANG I.