Mulvany M J
Blood Vessels. 1983;20(1):1-22. doi: 10.1159/000158455.
This review summarizes some of the evidence pointing to the existence of vascular abnormalities in the spontaneously hypertensive rat (SHR) and the extent to which such abnormalities could be responsible for the elevated blood pressure in this animal. Compared with its genetic normotensive control, the Wistar-Kyoto rat (WKY), the adult SHR has an increased total peripheral resistance (TPR). Many factors appear to contribute to the increased TPR, including an active rarefication of the vascular bed and a general constriction of the vasculature. There is evidence that the general constriction is due to structural differences in the resistance vessels, to abnormally high activation levels (i.e. increased sympathetic nerve activity), and to abnormal excitation-contracting coupling within the vasculature itself (i.e. increased noradrenaline sensitivity of the vascular smooth muscle cells). Age studies and studies of the effects of antihypertensive treatment suggest that both structural and excitation-contraction abnormalities may be present before the onset of hypertension.
本综述总结了一些指向自发性高血压大鼠（SHR）存在血管异常的证据，以及这些异常在多大程度上可能导致该动物血压升高。与基因正常血压对照的Wistar-Kyoto大鼠（WKY）相比，成年SHR的总外周阻力（TPR）增加。许多因素似乎导致了TPR的增加，包括血管床的主动稀疏和血管系统的普遍收缩。有证据表明，普遍收缩是由于阻力血管的结构差异、异常高的激活水平（即交感神经活动增加）以及血管系统本身异常的兴奋-收缩偶联（即血管平滑肌细胞对去甲肾上腺素的敏感性增加）。年龄研究和抗高血压治疗效果研究表明，在高血压发作之前可能就已经存在结构和兴奋-收缩异常。
