Role of the arterial baroreflex in 5-HT1A receptor agonist-mediated sympathoexcitation following hypotensive hemorrhage.
Role of the arterial baroreflex in 5-HT1A receptor agonist-mediated sympathoexcitation following hypotensive hemorrhage.
复制标题
动脉压力反射在低血压出血后 5-HT1A 受体激动剂介导的交感兴奋中的作用。
DOI：
10.1152/ajpregu.00671.2005
复制
发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Scrogin,Karie
中科院分区：
文献类型：
--
作者：
Osei-Owusu,Patrick;Scrogin,Karie
5-HT 1A受体激动剂能迅速恢复脑出血清醒大鼠的血压和交感神经活性。5-HT 1A受体激活也已显示在麻醉猫中产生心脏交感神经的压力感受器依赖性脉冲同步放电的稳健增加。为了确定5-HT 1A受体激动剂是否通过促进动脉压力感受器反射来逆转交感神经活性的抑制，在经历窦主动脉压力感受器去神经和随后的肿胀性出血的雄性Sprague-Dawley大鼠中评估了5-HT 1A受体激动剂8-OH-DPAT的作用。8-OH-DPAT在老龄动物中产生快速升压和交感兴奋反应，这些反应被窦弓去神经（SAD）减弱，但未被阻断（+49 ± 4 vs. +37 ± 4 mmHg; +165 ± 30 vs. +92 ± 24%基线，P< 0.01）。交感神经活动的频谱分析表明，SAD消除了8-羟基-2-（二正丙基氨基）-四氢萘（8-OH-DPAT）介导的脉冲同步（13 ± 1 vs. 5 ± 1%总功率，完整与SAD大鼠，P< 0.01）和Mayer波相关爆发（18 ± 3 vs. 8 ± 1%总功率，P< 0.05）的增加。然而，8-OH-DPAT继续增加SAD动物的总功率（+72 ± 22 vs. −63 ± 7%出血前总功率，P< 0.05）和呼吸频率下的功率（35 ± 2 vs. 25 ± 4%总功率）。这些数据表明，8-OH-DPAT的交感神经兴奋作用的充分表达需要功能性动脉压力感受器反射。然而，一部分的效果是由于激活动脉压力反射独立的交感神经通路。
5-HT1A-receptor agonists rapidly restore blood pressure and sympathetic activity in conscious rats subjected to hypotensive hemorrhage. 5-HT1A-receptor activation has also been shown to produce a robust increase in baroreceptor-dependent, pulse-synchronous firing of cardiac sympathetic nerves in anesthetized cats. To determine whether 5-HT1A-receptor agonists reverse hemorrhage-induced suppression of sympathetic activity through facilitation of the arterial baroreflex, the effects of the 5-HT1A-receptor agonist, 8-OH-DPAT, were assessed in male Sprague-Dawley rats subjected to sinoaortic baroreceptor denervation and subsequent hypotensive hemorrhage. 8-OH-DPAT produced rapid pressor and sympathoexcitatory responses in hemorrhaged animals that were attenuated, but not blocked, by sinoaortic denervation (SAD) (+49 ± 4 vs. +37 ± 4 mmHg; +165 ± 30 vs. +92 ± 24% baseline,P< 0.01). Spectral analysis of sympathetic activity showed that SAD abolished the 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT)-mediated increases in pulse-synchronous (13 ± 1 vs. 5 ± 1% total power for intact vs. SAD rats,P< 0.01) and Mayer wave-related bursting (18 ± 3 vs. 8 ± 1% total power,P< 0.05). However, 8-OH-DPAT continued to increase total power (+72 ± 22 vs. −63 ± 7% prehemorrhage total power,P< 0.05) and power at the respiratory frequency (35 ± 2 vs. 25 ± 4% total power) in SAD animals. These data indicate that full expression of the sympathoexcitatory effect of 8-OH-DPAT requires a functional arterial baroreflex. However, a portion of the effect is due to activation of arterial baroreflex-independent sympathetic pathways.