Vincent H H, Boomsma F, Man in 't Veld A J, Schalekamp M A
J Hypertens. 1986 Apr;4(2):255-60. doi: 10.1097/00004872-198604000-00018.
The possibility that sympathetic pressor responses are modulated by adrenaline-mediated facilitation of neuronal noradrenaline release was explored in 17 subjects with borderline hypertension. Infusion of adrenaline, which raised plasma adrenaline by a factor of 8 to 9, augmented the rise in systolic and diastolic arterial pressure induced by standardized cold pressor and isometric exercise tests. The heart rate response to these tests was not affected. When a low dose of propranolol was given on top of the adrenaline infusion before the cold pressor test, the blood pressure response to cold exposure was not different from the response observed when the test was performed during saline infusion. Plasma noradrenaline was higher during adrenaline infusion then during saline infusion, both before and after the cold pressor and isometric exercise tests, and the effect of adrenaline on plasma noradrenaline was antagonized by propranolol. These observations are consistent with the hypothesis that stress levels of circulating adrenaline may amplify sympathetic pressor responses by facilitation of the release of transmitter noradrenaline.
在17名临界高血压患者中,探讨了交感缩血管反应是否受肾上腺素介导的神经元去甲肾上腺素释放促进作用调节的可能性。输注肾上腺素使血浆肾上腺素升高8至9倍,增强了标准化冷加压和等长运动试验诱导的收缩压和舒张压升高。这些试验引起的心率反应未受影响。在冷加压试验前,在输注肾上腺素的基础上给予低剂量普萘洛尔时,对冷暴露的血压反应与输注生理盐水期间进行试验时观察到的反应无差异。在冷加压试验和等长运动试验前后,输注肾上腺素期间的血浆去甲肾上腺素均高于输注生理盐水期间,普萘洛尔可拮抗肾上腺素对血浆去甲肾上腺素的作用。这些观察结果与以下假设一致,即循环肾上腺素的应激水平可能通过促进递质去甲肾上腺素的释放来放大交感缩血管反应。