TRANSITION FROM HIGH CARDIAC-OUTPUT TO ELEVATED VASCULAR-RESISTANCE IN HYPERTENSION
TRANSITION FROM HIGH CARDIAC-OUTPUT TO ELEVATED VASCULAR-RESISTANCE IN HYPERTENSION
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DOI：
10.1016/0002-8703(88)90557-1
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发表时间：
1988-08-01
影响因子：
4.8
通讯作者：
JULIUS, S
中科院分区：
文献类型：
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作者：
JULIUS, S
高血压的早期阶段（边缘性高血压）的特点是由于交感神经过度驱动和心脏副交感神经抑制减少而引起的血液循环亢进。在后期，心输出量变得正常，但高血压仍然是神经源性的，持续的药物副交感神经、β-和α-肾上腺素能抑制使血压正常化这一事实证明了这一点。在该过程的这两个阶段，血浆去甲肾上腺素值都会升高。这些患者还表现出特有的行为模式；他们外向、顺从，但会感到无法表达的愤怒，并经常怀有敌意。在高血压晚期，心输出量正常，总外周阻力升高。这种血流动力学转变可以通过对血压升高的继发反应来解释。由于受体反应性改变和心脏顺应性降低，心脏的反应性降低，而小动脉的反应性由于血管肥大而增加，从而导致壁与管腔比率的变化。然而，一项观察结果无法解释：高血压后期血浆去甲肾上腺素不升高。我们提出了一个新的概念框架来解释高血压病程中血浆去甲肾上腺素升高的消失。该概念基于在神经源性升压反应期间使用各种受体阻断剂的广泛观察。血压反应总是被保留，但血流动力学模式可以从高心输出量改变为高总外周阻力，反之亦然。中枢神经系统的“血压寻求行为”表明，中枢神经系统的负反馈与压力有关，与流量无关。如果中枢神经系统确实寻求在早期阶段通过心输出量升高来获得一定的压力并维持高血压，那么随着小动脉结构的变化以及小动脉变得高反应性，可以通过较少的交感神经驱动来实现相同的血压升高，并且血浆去甲肾上腺素值恢复到正常范围。
The early phase of hypertension (borderline hypertension) is characterized by a hyperkinetic circulation caused by excessive sympathetic drive and decreased parasympathetic inhibition to the heart. In later phases the cardiac output becomes normal, but the hypertension is still neurogenic, as demonstrated by the fact that continued pharmacologic parasympathetic, β- and α-adrenergic inhibition normalizes the blood pressure. In both of these phases of the process, plasma norepinephrine values are elevated. These patients also show characteristic behavioral patterns; they are outward oriented, submissive, but experience unexpressed anger and frequently harbor hostile feelings. In late phases of hypertension the cardiac output is normal and the total peripheral resistance is elevated. This hemodynamic transition can be explained by a secondary response to elevated blood pressure. The heart becomes less responsive as a result of altered receptor responsiveness and decreased cardiac compliance, whereas the responsiveness of arterioles increases because of vascular hypertrophy, which leads to changes in the wall-to-lumen ratio. However, one observation eludes explanation: the absence of plasma norepinephrine elevation in later phases of hypertension. We propose a new conceptual framework to explain the disappearance of elevated plasma norepinephrine in the course of hypertension. The concept is based on a wide range of observations with the use of various receptor-blocking agents during neurogenic pressor responses. Invariably, the blood pressure response is preserved, but the hemodynamic pattern can be altered from a high cardiac output to high total peripheral resistance or vice versa. The “blood pressure-seeking behavior” of the central nervous system suggests that the negative feedback to the central nervous system ispressureand notflowrelated. If the central nervous system indeed seeks to obtain a certain pressure and maintains the high blood pressure in early phases by an elevation in cardiac output, later as structural arteriolar changes evolve and the arterioles become hyperresponsive, the same blood pressure elevation could be achieved with less sympathetic drive, and the plasma norepinephrine values return to the normal range.