Buñag R, Eferakeya A
Cardiovasc Res. 1976 Nov;10(6):663-71. doi: 10.1093/cvr/10.6.663.
If the posterior hypothalamus contributes to elevate blood pressure in hypertension by increasing sympathetic vasomotor activity, then lesions of the posterior hypothalamus should lower blood pressure more in hypertensive than in normotensive rats. To test this hypothesis without complications caused by anaesthesia, aortic pressures were recorded from indwelling catheters in awake rats before and after selective hypothalamic destruction. In normotensive rats rats, bilateral lesions of the medial areas of the posterior hypothalamus always lowered blood pressure while those in the anterior hypothalamus slightly increased it. Heart rate responses varied widely and did not seem to contribute to the blood pressure changes. Posterior hypothalamic lesions of approximately the same size had significantly greater hypotensive after-effects in renal and spontaneously hypentensive rats than in normotensive or Doca hypentensive ones. These results imply that sympathetic overactivity emanating from posterior hypothalamic centres contributes to the blood pressure elevation in spontaneous or chronic renal hypentension but not in Doca hypertension. However, because of inherent weaknesses in the 'lesion method' and the complexity of blood pressure regulation in awake animals, other explanations are possible.
如果下丘脑后部通过增加交感缩血管活动导致高血压患者血压升高，那么下丘脑后部损伤在高血压大鼠中降低血压的幅度应大于正常血压大鼠。为了在无麻醉并发症的情况下验证这一假设，在选择性下丘脑破坏前后，通过植入清醒大鼠体内的导管记录主动脉血压。在正常血压大鼠中，下丘脑后部内侧区域的双侧损伤总是会降低血压，而下丘脑前部的损伤则会使其略有升高。心率反应差异很大，似乎与血压变化无关。大小大致相同的下丘脑后部损伤在肾性和自发性高血压大鼠中产生的降压后效应，比在正常血压或去氧皮质酮性高血压大鼠中显著更大。这些结果表明，下丘脑后部中心发出的交感神经过度活动导致自发性或慢性肾性高血压患者血压升高，但去氧皮质酮性高血压患者并非如此。然而，由于“损伤法”存在固有缺陷以及清醒动物血压调节的复杂性，其他解释也是有可能的。
