Peripheral neurogenic factors in acute and chronic alterations of arterial pressure.
Peripheral neurogenic factors in acute and chronic alterations of arterial pressure.
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DOI：
10.1161/01.res.53.2.121
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发表时间：
1983-08
影响因子：
20.1
通讯作者：
B. Zimmerman
中科院分区：
文献类型：
--
作者：
B. Zimmerman
多年来，人们已经很好地认识到，全身动脉血压的控制作用于中枢和外周神经部位。最近，很多注意力都集中在动脉血压调节的中心成分上，并且已经有许多综述致力于该主题（参见Brody等人，1980;查尔默斯，1975;希尔顿和斯派尔，1980;帕尔科维奇和扎博尔斯基，1977）。较少强调的是外周神经对血压调节相关的血管张力的影响。在评估外围或中心因素的相对重要性时遇到的困难之一是独立研究它们的方法不精确。暗示由于某些干预而引起的外周神经源性功能的改变常常被中枢影响所混淆。如果检查交感神经功能的代表性变化，则提供这种情况的示例。由于DOCA-盐处理导致的心脏组织中去甲肾上腺素含量的降低最初归因于外周肾上腺素能神经的神经囊泡的储存能力的缺陷（Krakoff等人，1967年）。然而，进一步的实验表明，含量降低是由于中枢交感神经流出增加引起的去甲肾上腺素周转增加（De Champlain et al.，1969; Haeusler等人，1972;货车Ameringen等人，1977; Giachetti等人，1979年）。这种中枢机制是目前对DOCA-盐高血压中肾上腺素能储存抑制的观察给出的解释，而不是外周神经损伤的解释（Giachetti等人，1979年）。研究药物对中枢神经功能作用的方法也存在一些困难。描述激动剂或拮抗剂对中枢血管功能的作用的常用方法是将药物注入脑室系统，脑室内或脑池内。由于进行这种输注的体积相对较小，这些药剂常常达到非生理学的高浓度，因此必须谨慎地从这些实验中得出结论。还可通过椎动脉和颈动脉进入中央血管区。然而，药物，即使以低剂量给药，也会再循环进入全身血管床，并可能产生直接影响。必须包括对照实验，以建立明确的中心效应。监测中枢交感神经放电的有用手段是通过记录节前交感神经活动（Bronk等人，1936年）。这种技术通常用于急性实验，但很少用于有意识的动物。需要更精确的方法来量化在更生理条件下中枢和外周因素对血管神经源性功能的相对参与，例如，清醒的动物
FOR MANY years it has been well apreciated that the control of systemic arterial blood pressure is exerted at central as well as peripheral neural sites. Much attention has been directed recently at the central component of arterial blood pressure regulation, and numerous reviews have been devoted to this subject (see Brody et al., 1980; Chalmers, 1975; Hilton and Spyer, 1980; Palkovits and Zaborszky, 1977). Less emphasis has been placed on peripheral neurogenic influences on vascular tone relating to blood pressure regulation. One of the difficulties encountered when evaluating relative importance of peripheral or central factors is the imprecise methodology for studying them independently. Implicating a change in peripheral neurogenic function due to some intervention is often confounded by central influences. An example of this is provided if a representative change in sympathetic neural function is examined. A decrease in norepinephrine content in cardiac tissue due to DOCA-salt treatment was originally attributed to a defect in the storage capacity of the nerve vesicles of peripheral adrenergjc nerves (Krakoff et al., 1967). However, further experimentation revealed that the decreased content was due to increased turnover of norepinephrine brought about by an increase in central sympathetic outflow (De Champlain et al., 1969; Haeusler et al., 1972; Van Ameringen et al., 1977; Giachetti et al., 1979). This central mechanism is the explanation currently given for the observation of depressed adrenergic storage in DOCA-salt hypertension, rather than that of peripheral nerve impairment (Giachetti et al., 1979). Methods to study drug actions on central neurogenic function also present some difficulties. A common means to delineate the effects of agonists or antagonists upon central vasomotor function is to infuse the agents into the ventricular system, either intracerebroventricularly or intracisternally. Because of the relatively small volumes into which such infusions are made, unphysiologically high concentrations of these agents are often reached, and therefore conclusions drawn from these experiments must be made cautiously. Access to the central vasomotor areas via the vertebral and carotid arteries is also utilized. However, drugs, even if given in low doses, recirculate into the systemic vascular beds and may exert direct effects. Control experiments must be included to establish a definite central effect. A useful means of monitoring the central sympathetic discharge is by recording preganglionic sympathetic nerve activity (Bronk et al., 1936). This technique is used routinely in acute experiments but is applied less often to conscious animals. More precise methods are needed to quantify the relative participation of central and peripheral factors on vascular neurogenic function under more physiological conditions, e.g., in awake animals.