Lokhandwala M F, Eikenburg D C
Life Sci. 1983 Oct 17;33(16):1527-42. doi: 10.1016/0024-3205(83)90693-8.
The ability of blood vessels to constrict to a given stimulus is significantly increased in spontaneously hypertensive rats (SHR). Such an increase in the vasoconstrictor responsiveness contributes to the elevated peripheral vascular resistance noted in SHR. The present review discusses evidence in support of the concept that an increased release of norepinephrine during sympathetic nerve stimulation may contribute to the increase in vasoconstrictor responsiveness and, subsequently, to an increase in vascular resistance in the SHR. Several studies suggest that the exocytotic release of norepinephrine from sympathetic nerves may be altered by endogenously occurring neurohumoral substances which produce their effects by interacting with presynaptic receptors located on postganglionic sympathetic nerves. Therefore, it is postulated that alterations in presynaptic regulation of norepinephrine release, resulting from changes in the functioning of one or more of these presynaptic receptors, may lead to a greater release of norepinephrine in the SHR. This review summarizes the results of studies evaluating presynaptic receptor mechanisms and norepinephrine release in the SHR. These studies suggest that norepinephrine release during sympathetic nerve stimulation is greater in the SHR and that alterations in some of the presynaptic receptor mechanisms may be responsible for this phenomenon.
自发性高血压大鼠（SHR）血管对特定刺激的收缩能力显著增强。这种血管收缩反应性的增加导致了SHR外周血管阻力升高。本综述讨论了支持以下概念的证据：交感神经刺激期间去甲肾上腺素释放增加可能导致血管收缩反应性增加，进而导致SHR血管阻力增加。多项研究表明，交感神经去甲肾上腺素的胞吐释放可能会被内源性神经体液物质改变，这些物质通过与节后交感神经上的突触前受体相互作用发挥作用。因此，推测一种或多种这些突触前受体功能的改变导致去甲肾上腺素突触前释放调节的改变，可能会导致SHR中去甲肾上腺素释放增加。本综述总结了评估SHR中突触前受体机制和去甲肾上腺素释放的研究结果。这些研究表明，SHR交感神经刺激期间去甲肾上腺素释放更多，一些突触前受体机制的改变可能是导致这一现象的原因。
