Watson A J, Di Pette D
Clin Sci (Lond). 1985 Nov;69(5):637-40. doi: 10.1042/cs0690637.
Baroreflex sensitivity and pressor responsiveness to exogenous noradrenaline, angiotensin II and arginine vasopressin were determined in a rat model of uraemia. The slope of the regression line relating delta heart rate to delta blood pressure after phenylephrine administration was significantly less in the renal failure group than the normal control group, indicating a reduction of baroreflex sensitivity in the setting of uraemia. The pressor response to noradrenaline and angiotensin II was significantly less in the renal failure group whereas there was no difference in delta blood pressure on administration of arginine vasopressin. It is concluded that diminished baroreflex sensitivity does not contribute to the pathogenesis of hypertension in uraemia by the hypothesized mechanism of allowing the pressor effect of endogenous pressor substances to go unbuffered.
在尿毒症大鼠模型中测定了压力反射敏感性以及对外源性去甲肾上腺素、血管紧张素II和精氨酸加压素的升压反应。给予去氧肾上腺素后，肾衰竭组中与心率变化相关的血压变化回归线斜率显著低于正常对照组，这表明在尿毒症情况下压力反射敏感性降低。肾衰竭组对去甲肾上腺素和血管紧张素II的升压反应显著降低，而给予精氨酸加压素后血压变化无差异。得出的结论是，压力反射敏感性降低并非通过所假设的使内源性升压物质的升压作用未得到缓冲的机制导致尿毒症高血压的发病。
