Attenuation of aortic baroreflex responses by microinjections of endomorphin-2 into the rostral ventrolateral medullary pressor area of the rat
Attenuation of aortic baroreflex responses by microinjections of endomorphin-2 into the rostral ventrolateral medullary pressor area of the rat
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DOI：
10.1152/ajpregu.00007.2005
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发表时间：
2005-07-01
影响因子：
2.8
通讯作者：
Sapru, HN
中科院分区：
文献类型：
--
作者：
Kasamatsu, K;Sapru, HN
已证实在延髓腹外侧加压区(RVLM)周围的一般区域存在Mu-阿片受体和内吗啡。这项研究是为了验证这样一种假设，即RVLM中的内吗啡可能在调节心血管功能方面具有调节作用。在乌拉坦麻醉的雄性Wistar大鼠上记录血压和心率。单侧RVLm内微量注射内吗啡-2(0.0125-0.5mmo1/L)可引起平均动脉压(16-30 mm Hg)和心率(12-36次/m in)的降低，持续2-4 m in。心动过缓不是通过调节的。由于预先微量注射纳洛酮(1 mmol/L)可阻断内吗啡肽-2的作用，因此内吗啡肽-2的作用是通过Mu-阿片受体介导的，其阻断作用可持续15-20min。单侧主动脉神经刺激S 30次(频率5、10、25次/S，每次0.5V，持续时间1ms)可引起降压和心动过缓反应。微量注射内吗啡-2(0.2和0.4 mm o l/L)可显著减弱上述反应。内吗啡-2对压力感受性反射的抑制作用可被预先微量注射纳洛酮所阻断。单独微量注射纳洛酮并不影响基线血压和心率或压力感受器反射反应。这些结果表明，内吗啡-2可引起降压和心动过缓反应，并抑制压力感受器反射功能。这些效应与阿片肽对RVLM神经元的超极化效应是一致的。
The presence of mu-opioid receptors and endomorphins has been demonstrated in the general area encompassing the rostral ventrolateral medullary pressor area ( RVLM). This investigation was carried out to test the hypothesis that endomorphins in the RVLM may have a modulatory role in regulating cardiovascular function. Blood pressure and heart rate (HR) were recorded in urethane-anesthetized male Wistar rats. Unilateral microinjections of endomorphin-2 (0.0125-0.5 mmol/l) into the RVLM elicited decreases in mean arterial pressure (16-30 mmHg) and HR (12-36 beats/min), which lasted for 2-4 min. Bradycardia was not vagally mediated. The effects of endomorphin-2 were mediated via mu-opioid receptors because prior microinjections of naloxonazine (1 mmol/l) abolished these responses; the blocking effect of naloxonazine lasted for 15-20 min. Unilateral stimulations of aortic nerve for 30 s (at frequencies of 5, 10, and 25 pulses/s; each pulse 0.5 V and 1-ms duration) elicited depressor and bradycardic responses. These responses were significantly attenuated by microinjections of endomorphin-2 (0.2 and 0.4 mmol/l). The inhibitory effect of endomorphin-2 on baroreflex responses was prevented by prior microinjections of naloxonazine. Microinjections of naloxonazine alone did not affect either baseline blood pressure and HR or baroreflex responses. These results indicate that endomorphin-2 elicits depressor and bradycardic responses and inhibits baroreflex function when injected into the RVLM. These effects are consistent with the known hyperpolarizing effect of opioid peptides on RVLM neurons.