Popovici D, Cristoveanu A, Stefănescu A M, Juvină E
Endocrinologie. 1980 Oct-Dec;18(4):225-34.
The endocrine system becomes involved in the physiopathologic mechanisms of essential arterial hypertension (EAH) by the interference of hormones with the pressor and depressor substances. A "depressor" pharmacodynamic model with beta-blockers based on the variations of hormone-dependent data offers a series of characteristics for assessing the vasoconstrictive and volemic components, evolution (accelerated for instance) and treatment. Hormone data are also useful for avoiding errors and for increasing the efficiency and control of the therapy. It is not uncommon for EAH to become endocrine-dependent, for instance: increase in aldosterone secretion by activation of the renin-angiotensin (RA) system or of the hypophysis- corticoadrenal system and the adreno-sympathetic system, transforms the relatively "benign" evolution of EAH into an "accelerated" one. The incidence of hyperreactive corticoadrenal (with or without altered steroidogenesis), corticoadrenal hyperplasia or adenoma, is in reality higher than commonly diagnosed.
内分泌系统通过激素对升压和降压物质的干扰而参与原发性高血压（EAH）的病理生理机制。基于激素依赖性数据变化的β受体阻滞剂“降压”药效学模型提供了一系列用于评估血管收缩和血容量成分、病情进展（例如加速进展）及治疗的特征。激素数据对于避免错误以及提高治疗的效率和可控性也很有用。EAH转变为内分泌依赖性的情况并不少见，例如：肾素 - 血管紧张素（RA）系统、垂体 - 肾上腺皮质系统及肾上腺 - 交感神经系统激活导致醛固酮分泌增加，会使EAH相对“良性”的进展转变为“加速”进展。实际上，高反应性肾上腺皮质（无论类固醇生成是否改变）、肾上腺皮质增生或腺瘤的发生率高于通常诊断的情况。
