Hamada M, Shigematsu Y, Mukai M, Kazatani Y, Kokubu T, Hiwada K
Second Department of Internal Medicine, Ehime University School of Medicine, Japan.
Hypertension. 1995 Feb;25(2):266-71. doi: 10.1161/01.hyp.25.2.266.
To elucidate whether a difference in blood pressure reactivity exists between patients with pheochromocytoma (n = 8) and pseudopheochromocytoma (n = 22), we evaluated blood pressure changes during a Valsalva maneuver and baroreceptor reflex sensitivity. We also examined the effects of propranolol and prazosin on blood pressure reactivity during a Valsalva maneuver in patients with pseudopheochromocytoma. Pseudopheochromocytoma was defined as a paroxysmal rise in blood pressure accompanying pheochromocytoma-like symptoms and normal catecholamine values. The difference in systolic blood pressure between phase IV of the Valsalva maneuver and baseline (delta SBP) was markedly smaller in the pheochromocytoma patients (8.4 +/- 18.4 mm Hg) than in the essential hypertension patients (n = 30, 30.9 +/- 19.4 mm Hg) and normotensive control subjects (n = 10, 31.3 +/- 11.4 mm Hg), whereas delta SBP in the pseudopheochromocytoma patients (77.8 +/- 11.2 mm Hg) was markedly greater than in the other three groups. delta SBP was markedly suppressed by the administration of both propranolol and prazosin. Baroreceptor reflex sensitivity index was lower in the pheochromocytoma group than in the other three groups. In conclusion, blood pressure reactivity responses to a Valsalva maneuver are disparate between pheochromocytoma and pseudopheochromocytoma. The high blood pressure reactivity to a Valsalva maneuver in pseudopheochromocytoma is due to hyperactivity in both beta- and alpha 1-adrenergic receptor functions, and the low blood pressure reactivity to a Valsalva maneuver in pheochromocytoma seems to be mainly due to the desensitization of both adrenergic systems associated with chronic catecholamine excess. In addition, the impaired baroreceptor function in pheochromocytoma is partially responsible for it.
为了阐明嗜铬细胞瘤患者(n = 8)和假嗜铬细胞瘤患者(n = 22)之间是否存在血压反应性差异,我们评估了瓦尔萨尔瓦动作期间的血压变化以及压力感受器反射敏感性。我们还研究了普萘洛尔和哌唑嗪对假嗜铬细胞瘤患者瓦尔萨尔瓦动作期间血压反应性的影响。假嗜铬细胞瘤被定义为伴有嗜铬细胞瘤样症状和正常儿茶酚胺值的血压阵发性升高。瓦尔萨尔瓦动作第四阶段与基线之间的收缩压差异(ΔSBP)在嗜铬细胞瘤患者中(8.4±18.4 mmHg)明显小于原发性高血压患者(n = 30,30.9±19.4 mmHg)和血压正常的对照受试者(n = 10,31.3±11.4 mmHg),而假嗜铬细胞瘤患者的ΔSBP(77.8±11.2 mmHg)明显大于其他三组。普萘洛尔和哌唑嗪的给药均显著抑制了ΔSBP。嗜铬细胞瘤组的压力感受器反射敏感性指数低于其他三组。总之,嗜铬细胞瘤和假嗜铬细胞瘤对瓦尔萨尔瓦动作的血压反应性不同。假嗜铬细胞瘤对瓦尔萨尔瓦动作的高血压反应性是由于β和α1肾上腺素能受体功能亢进,而嗜铬细胞瘤对瓦尔萨尔瓦动作的低血压反应性似乎主要是由于与慢性儿茶酚胺过量相关的两种肾上腺素能系统脱敏。此外,嗜铬细胞瘤中压力感受器功能受损对此也有部分作用。