Baroreflex modulation by angiotensins at the rat rostral and caudal ventrolateral medulla
Baroreflex modulation by angiotensins at the rat rostral and caudal ventrolateral medulla
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DOI：
10.1152/ajpregu.00852.2004
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发表时间：
2006-04-01
影响因子：
2.8
通讯作者：
Campagnole-Santos, MJ
中科院分区：
文献类型：
--
作者：
Alzamora, AC;Santos, RAS;Campagnole-Santos, MJ
血管紧张素对大鼠延髓头端和尾侧腹外侧压力感受性反射的调节。Am J Physiol Regul Integr Comp Physiol 290：R1027-R1034，2006年。首次出版于2005年11月23日; doi：10.1152/ajpregu。00852.2004. - 我们测定了将ANG-（1 - 7）和ANG II微量注射到控制循环的延髓的两个关键区域[延髓头端和尾侧腹外侧区（分别为RVLM和CVLM）]对麻醉大鼠心率（HR）的压力感受性反射控制的影响。反射性心动过缓和心动过速引起的平均动脉压的增加和减少，分别由静脉注射苯肾上腺素和硝普钠。在RVLM微量注射（分别为11 +/- 0.8和10 +/- 2 mmHg）后，ANG-（1 - 7）和ANG II（25 pmol）的升压作用并不伴随HR的一致变化。此外，RVLM微量注射这些血管紧张素肽并不改变压力感受性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产生低血压（分别为-11 +/- 1.5和-11 +/- 1.9 mmHg），同样没有伴随HR的显著变化。CVLM微量注射血管紧张素可引起HR压力反射控制的不同变化，ANG-（1 - 7）可减弱HR压力反射性心动过缓（0.26 +/- 0.06 ms/mmHg vs.治疗前0.42 +/- 0.08 ms/mmHg）并促进压力反射性心动过速（治疗前为0.86 +/- 0.19 ms/mmHg vs. 0.42 +/- 0.10 ms/mmHg）; ANG II产生相反的效果，衰减性压力反射性心动过速（治疗前0.09 +/- 0.06 ms/mmHg vs. 0.31 +/- 0.07 ms/mmHg）并促进压力反射性心动过缓（治疗前为0.67 +/- 0.16 ms/mmHg vs. 0.41 +/- 0.05 ms/mmHg）。ANG Ⅱ和ANG-（1 - 7）对压力感受性反射敏感性的调节作用可被外周注射甲基阿托品完全阻断。这些结果表明，血管紧张素II和血管紧张素-（1 - 7）在CVLM产生的压力反射控制的HR的差异调制，可能通过对心脏的副交感神经驱动的不同影响。
Baroreflex modulation by angiotensins at the rat rostral and caudal ventrolateral medulla. Am J Physiol Regul Integr Comp Physiol 290: R1027-R1034, 2006. First published November 23, 2005; doi: 10.1152/ajpregu. 00852.2004. - 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.