Shepherd J T
Mayo Clinic and Foundation, Rochester, Minnesota 55905.
J Hypertens Suppl. 1990 Dec;8(7):S15-27.
Polygenetic predisposition is a key factor in the multifactorial disorders of primary hypertension. It is suggested that endothelial cell abnormalities are the major factors responsible for the increase in total systemic vascular resistance that leads to an elevation in arterial blood pressure. Thus, resetting of the arterial baroreceptors could be a consequence of endothelial-mediated changes in mechano-electrical transduction in the arterial mechanoreceptors. In consequence, inhibition of the vasomotor centers would be diminished and the resulting neurohumoral excitation would constrict the systemic resistance blood vessels. Later, as left ventricular hypertrophy develops, the inhibitory input of the cardiac mechanoreceptors is also reduced. In normal endothelial cells there is a predominant formation and release of vascular smooth muscle relaxing and growth-inhibiting factors. However, it is proposed that genetic changes lead to a predominate formation of endothelium-derived contracting factors and mitogens. The former would augment the neurohumoral vasoconstriction. The latter, aided by the increased arterial pressure and the augmented output of norepinephrine, would lead to structural alterations in the arterial vessels, thus reducing the lumen area, amplifying the vasoconstrictor response to contractile agents and limiting vasodilation. In this way the hypertension would be perpetuated.
多基因易感性是原发性高血压这一多因素疾病的关键因素。有研究表明，内皮细胞异常是导致总全身血管阻力增加从而引起动脉血压升高的主要因素。因此，动脉压力感受器的重置可能是内皮介导的动脉机械感受器机械电转换变化的结果。结果，血管运动中枢的抑制作用会减弱，由此产生的神经体液兴奋会使全身阻力血管收缩。后来，随着左心室肥厚的发展，心脏机械感受器的抑制性输入也会减少。在正常内皮细胞中，主要形成并释放血管平滑肌舒张因子和生长抑制因子。然而，有人提出基因变化会导致内皮衍生的收缩因子和有丝分裂原占主导形成。前者会增强神经体液性血管收缩。后者在动脉压升高和去甲肾上腺素输出增加的辅助下，会导致动脉血管结构改变，从而减小管腔面积，增强血管对收缩剂的血管收缩反应并限制血管舒张。通过这种方式，高血压得以持续。
