Heesch C M, Bishop V S
Circ Res. 1982 Sep;51(3):391-9. doi: 10.1161/01.res.51.3.391.
The purpose of this study was to examine the role of carotid sinus and cardiopulmonary mechanoreceptors in the reflex control of adrenal medullary catecholamine secretion. Afferent input from carotid sinus and cardiopulmonary mechanoreceptors was decreased by carotid occlusion or cervical vagal cold block, respectively. Increases in arterial pressure were significantly greater when either intervention was tested in the presence of the other, with the role of the carotid sinus baroreflex being dominant. Neither carotid occlusion nor vagal cold block resulted in a significant increase in plasma epinephrine or norepinephrine concentrations. However, carotid occlusion during vagal block caused a significant increase in plasma epinephrine (+87%) and norepinephrine concentrations (+128%). Likewise, vagal block during carotid occlusion increased plasma epinephrine (+82%) and norepinephrine concentrations (+73%). Similar experiments performed in a group of chemically sympathectomized animals (pre-treated with 50 mg/kg 6-hydroxydopamine) indicted that adrenal medullary norepinephrine as well as epinephrine release could be modulated by the carotid sinus and cardiopulmonary reflexes. Mean arterial blood pressure and heart rate were significantly lower in 6-hydroxydopamine-treated animals, compared with untreated controls. Although of lesser magnitude, responses to carotid occlusion and vagal block in 6-hydroxydopamine-treated animals were qualitatively similar to those in untreated animals. Plasma catecholamine concentrations did not increase from either manipulation. However, when the second manipulation was added to the first, significant increases occurred. We conclude from these data that both the carotid sinus and cardiopulmonary reflexes modulate the release of adrenal catecholamines. An interaction between the two reflexes exists whereby the influence of one reflex on catecholamine secretion is apparent only in the absence of the other input.
本研究的目的是探讨颈动脉窦和心肺机械感受器在肾上腺髓质儿茶酚胺分泌反射控制中的作用。分别通过颈动脉闭塞或颈迷走神经冷阻滞来减少来自颈动脉窦和心肺机械感受器的传入输入。当两种干预措施同时进行测试时,动脉压的升高显著更大,其中颈动脉窦压力反射起主导作用。颈动脉闭塞和迷走神经冷阻滞均未导致血浆肾上腺素或去甲肾上腺素浓度显著升高。然而,迷走神经阻滞期间的颈动脉闭塞导致血浆肾上腺素(+87%)和去甲肾上腺素浓度(+128%)显著升高。同样,颈动脉闭塞期间的迷走神经阻滞使血浆肾上腺素(+82%)和去甲肾上腺素浓度(+73%)升高。在一组化学性交感神经切除的动物(预先用50mg/kg 6-羟基多巴胺处理)中进行的类似实验表明,肾上腺髓质去甲肾上腺素以及肾上腺素的释放可受颈动脉窦和心肺反射调节。与未处理的对照组相比,6-羟基多巴胺处理的动物的平均动脉血压和心率显著更低。尽管幅度较小,但6-羟基多巴胺处理的动物对颈动脉闭塞和迷走神经阻滞的反应在性质上与未处理的动物相似。两种操作均未使血浆儿茶酚胺浓度升高。然而,当在第一种操作的基础上增加第二种操作时,就会出现显著升高。我们从这些数据得出结论,颈动脉窦和心肺反射均调节肾上腺儿茶酚胺的释放。两种反射之间存在相互作用,即一种反射对儿茶酚胺分泌的影响仅在没有另一种输入时才明显。