Bond R F, Johnson G
Experientia. 1985 May 15;41(5):607-9. doi: 10.1007/BF02007680.
The data suggest that rats genetically inbred to be hypertensive (SHR) are less able to compensate for hemorrhage and shock than their normotensive controls (WKY). Two reasons for this genetic dysfunction are: 1) SHRs seem to depend more on innervated alpha 1 than noninnervated alpha 2 adrenoreceptors for vasoconstriction; and 2) the vascular smooth muscle hypertrophy noted in SHRs may interfere with effective vasoconstriction.
数据表明,经基因近交培育而成的高血压大鼠(SHR)相比其血压正常的对照大鼠(WKY),在代偿出血和休克方面的能力较弱。这种基因功能障碍的两个原因是:1)SHR在血管收缩方面似乎更多地依赖于受神经支配的α1肾上腺素能受体而非不受神经支配的α2肾上腺素能受体;2)在SHR中观察到的血管平滑肌肥大可能会干扰有效的血管收缩。