Bond R F, Johnson G
Circ Shock. 1985;17(2):109-19.
Previous studies have suggested that spontaneously hypertensive rats (SHRs) are less able to tolerate the cardiovascular stress of hemorrhagic hypotension than normotensive WKYs. The present studies were designed to determine whether or not this deficiency on the part of the SHRs is related to a genetically derived inappropriate balance between the alpha 1- and alpha 2-adrenoreceptors in the peripheral vasculature. To answer this question, SHRs were divided into untreated controls and experimental rats, which were pretreated with either the relatively specific alpha 1-antagonist prazosin or the alpha 2-antagonist yohimbine. In another series, the adrenal medullae were removed 2-3 days before hemorrhage. The data indicate that alpha 1-receptor blockade might offer some degree of protection to SHRs subjected to hemorrhagic hypotension, whereas inhibition of the alpha 2-adrenoreceptors proved detrimental. We conclude that the innervated alpha 1-adrenoreceptors play a more dominant role in SHR blood pressure regulation than the extrasynaptic alpha 2-adrenoreceptors but that these alpha 1-receptors are unable to maintain the compensatory vasoconstrictor response as effectively as the alpha 2-adrenoreceptors.
先前的研究表明，自发性高血压大鼠（SHRs）比正常血压的WKY大鼠更难以耐受出血性低血压引起的心血管应激。本研究旨在确定SHRs的这种缺陷是否与外周血管系统中α1 - 和α2 - 肾上腺素能受体之间遗传衍生的不适当平衡有关。为了回答这个问题，将SHRs分为未处理的对照组和实验大鼠，实验大鼠分别用相对特异性的α1拮抗剂哌唑嗪或α2拮抗剂育亨宾进行预处理。在另一组实验中，在出血前2 - 3天摘除肾上腺髓质。数据表明，α1受体阻断可能为遭受出血性低血压的SHRs提供一定程度的保护，而抑制α2肾上腺素能受体则被证明是有害的。我们得出结论，在SHR血压调节中，受神经支配的α1肾上腺素能受体比突触外α2肾上腺素能受体发挥更主导的作用，但这些α1受体维持代偿性血管收缩反应的能力不如α2肾上腺素能受体有效。
