Judy W V, Watanabe A M, Murphy W R, Aprison B S, Yu P L
Hypertension. 1979 Nov-Dec;1(6):598-604. doi: 10.1161/01.hyp.1.6.598.
The genetic basis of hyperactivity of the sympathetic nervous system (SNA) in spontaneously hypertensive rats (SHR) was assessed by measuring SNA in animals derived from a backcross (BC) breeding program designed to isolate single gene differences causing changes in blood pressure. Selective breeding of the male hypertensive rats with inbred normotensive female Wistar/Lewis rats yielded progeny with a range of blood pressures, but whose group mean pressures were lower than the group mean pressures of the original SHR. Progressive generations had progressively lower group mean pressures. There was a positive correlation between SNA and mean arterial pressure in BC rats. These results indicate that the genetic defect in SHR may be abnormality in SNA, and the hypertension in these animals is a secondary result of this primary defect. Baroreceptor function was also assessed in SHR and in BC rats. In young (8 to 24 weeks old) SHR, baroreceptor function was similar to that in BC rats, whereas SNA was markedly increased. Only in older (24 to 40 weeks old) SHR was there an abnormality in the gain of baroreceptors. The development of hypertension in SHR therefore appears to be due to increased SNA resulting from a defect in the central nervous system. Changes in baroreceptor function are secondary to the hypertension and occur after the hypertension is established.
通过测量源于回交（BC）育种计划的动物的交感神经系统（SNA）活性，评估自发性高血压大鼠（SHR）交感神经系统活性亢进的遗传基础。该育种计划旨在分离导致血压变化的单基因差异。将雄性高血压大鼠与近交系正常血压雌性Wistar/Lewis大鼠进行选择性育种，产生了一系列血压的后代，但其群体平均血压低于原始SHR的群体平均血压。连续几代的群体平均血压逐渐降低。BC大鼠的SNA与平均动脉压之间存在正相关。这些结果表明，SHR的遗传缺陷可能是SNA异常，这些动物的高血压是这种原发性缺陷的继发结果。还评估了SHR和BC大鼠的压力感受器功能。在年轻（8至24周龄）的SHR中，压力感受器功能与BC大鼠相似，而SNA明显增加。仅在老年（24至40周龄）的SHR中，压力感受器的增益存在异常。因此，SHR高血压的发生似乎是由于中枢神经系统缺陷导致SNA增加。压力感受器功能的变化是高血压的继发结果，且在高血压形成后发生。
