Alzamora Andréia C, Santos Robson A S, Campagnole-Santos Maria J
Departamento de Fisiologia e Biofísica, Universidade Federal de Minas Gerais, Av. Antonio Carlos, 6627-ICB, UFMG, 31270-901, Belo Horizonte, MG, Brasil.
Am J Physiol Regul Integr Comp Physiol. 2006 Apr;290(4):R1027-34. doi: 10.1152/ajpregu.00852.2004. Epub 2005 Nov 23.
We determined the effect of microinjection of ANG-(1-7) and ANG II into two key regions of the medulla that control the circulation [rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively)] on baroreflex control of heart rate (HR) in anesthetized rats. Reflex bradycardia and tachycardia were induced by increases and decreases in mean arterial pressure produced by intravenous phenylephrine and sodium nitroprusside, respectively. The pressor effects of ANG-(1-7) and ANG II (25 pmol) after RVLM microinjection (11 +/- 0.8 and 10 +/- 2 mmHg, respectively) were not accompanied by consistent changes in HR. In addition, RVLM microinjection of these angiotensin peptides did not alter the bradycardic or tachycardic component of the baroreflex. CVLM microinjections of ANG-(1-7) and ANG II produced hypotension (-11 +/- 1.5 and -11 +/- 1.9 mmHg, respectively) that was similarly not accompanied by significant changes in HR. However, CVLM microinjections of angiotensins induced differential changes in the baroreflex control of HR. ANG-(1-7) attenuated the baroreflex bradycardia (0.26 +/- 0.06 ms/mmHg vs. 0.42 +/- 0.08 ms/mmHg before treatment) and facilitated the baroreflex tachycardia (0.86 +/- 0.19 ms/mmHg vs. 0.42 +/- 0.10 ms/mmHg before treatment); ANG II produced the opposite effect, attenuating baroreflex tachycardia (0.09 +/- 0.06 ms/mmHg vs. 0.31 +/- 0.07 ms/mmHg before treatment) and facilitating the baroreflex bradycardia (0.67 +/- 0.16 ms/mmHg vs. 0.41 +/- 0.05 ms/mmHg before treatment). The modulatory effect of ANG II and ANG-(1-7) on baroreflex sensitivity was completely abolished by peripheral administration of methylatropine. These results suggest that ANG II and ANG-(1-7) at the CVLM produce a differential modulation of the baroreflex control of HR, probably through distinct effects on the parasympathetic drive to the heart.
我们测定了向延髓中控制循环的两个关键区域[分别为头端和尾端腹外侧延髓（RVLM和CVLM）]微量注射血管紧张素-(1-7)（ANG-(1-7)）和血管紧张素II（ANG II）对麻醉大鼠心率（HR）压力反射控制的影响。分别通过静脉注射去氧肾上腺素和硝普钠使平均动脉压升高和降低来诱发反射性心动过缓和心动过速。RVLM微量注射后，ANG-(1-7)和ANG II（25 pmol）的升压作用（分别为11±0.8 mmHg和10±2 mmHg）并未伴随HR的一致变化。此外，向RVLM微量注射这些血管紧张素肽并未改变压力反射的心动过缓或心动过速成分。CVLM微量注射ANG-(1-7)和ANG II均产生了低血压（分别为-11±1.5 mmHg和-11±1.9 mmHg），同样未伴随HR的显著变化。然而，CVLM微量注射血管紧张素会引起压力反射对HR控制的不同变化。ANG-(1-7)减弱了压力反射性心动过缓（治疗前为0.42±0.08 ms/mmHg，治疗后为0.26±0.06 ms/mmHg）并增强了压力反射性心动过速（治疗前为0.42±0.10 ms/mmHg，治疗后为0.86±0.19 ms/mmHg）；ANG II产生了相反的效果，减弱了压力反射性心动过速（治疗前为0.31±0.07 ms/mmHg，治疗后为0.09±0.06 ms/mmHg）并增强了压力反射性心动过缓（治疗前为0.41±0.05 ms/mmHg，治疗后为0.67±0.16 ms/mmHg）。外周给予甲基阿托品可完全消除ANG II和ANG-(1-7)对压力反射敏感性的调节作用。这些结果表明，CVLM处的ANG II和ANG-(1-7)对压力反射对HR的控制产生不同的调节作用，可能是通过对心脏副交感神经驱动产生不同影响实现的。
