Smith R S, Albano J, Reid J L, Warren D J
Transplantation. 1983 Dec;36(6):666-70. doi: 10.1097/00007890-198336060-00016.
We have studied several factors that may cause hypertension in renal transplant recipients. Cardiac output measurements suggest that hypertension is maintained by an increase in total peripheral resistance. Plasma noradrenaline concentration was significantly higher in both normotensive and hypertensive patients than in matched normal subjects. Plasma noradrenaline rose significantly in response to head-up tilt in normotensive, but not in hypertensive, patients. Resting plasma renin activity was significantly higher in both groups of patients than in normal subjects, but there was no relationship between plasma renin activity and blood pressure. Plasma renin activity did not change in response to head-up tilt or isoprenaline infusion in the patients. The rise in arterial pressure during noradrenaline infusion was significantly greater in hypertensive than in normotensive patients. Regression analysis showed a significant relationship between the combination of total exchangeable sodium and the rise in mean arterial pressure during noradrenaline infusion with resting mean arterial pressure.
我们研究了肾移植受者中可能导致高血压的几个因素。心输出量测量结果表明,高血压是由总外周阻力增加维持的。正常血压和高血压患者的血浆去甲肾上腺素浓度均显著高于匹配的正常受试者。正常血压患者在头高位倾斜时血浆去甲肾上腺素显著升高,但高血压患者则不然。两组患者的静息血浆肾素活性均显著高于正常受试者,但血浆肾素活性与血压之间无相关性。患者在头高位倾斜或输注异丙肾上腺素后血浆肾素活性未发生变化。输注去甲肾上腺素期间高血压患者的动脉压升高显著大于正常血压患者。回归分析显示,总可交换钠与输注去甲肾上腺素期间平均动脉压升高与静息平均动脉压之间存在显著关系。