Reid J L
Department of Materia Medica, University of Glasgow, Scotland.
J Cardiovasc Pharmacol. 1988;12 Suppl 3:S114-20.
Hypertension, both essential and experimental is characterised by increased vascular resistance. This is in part structural, due to increases in the wall-to-lumen ratio secondary to vascular hypertrophy; however, functional increases in responses to neurohumoral stimuli also occur. The latter may be a consequence of hypertrophy or if a selective increase is observed, an indication of a primary underlying hypertensive mechanism. In essential hypertension, enhanced responsiveness to both angiotensin II and alpha-adrenoceptor agonists are seen. However, in some experimental models, more selective increased responses have been reported. The mechanism of alpha-adrenoceptor-mediated vascular smooth muscle contraction is reviewed and the role of inositol phosphates and diacylglycerol as second messengers is discussed. The precise mechanism of increased vascular responses in hypertension is still uncertain.
原发性高血压和实验性高血压均以血管阻力增加为特征。这部分是结构性的，是由于血管壁增厚继发血管腔狭窄导致壁腔比增加所致；然而，对神经体液刺激的反应性也会出现功能性增加。后者可能是肥大的结果，或者如果观察到选择性增加，则表明存在原发性潜在高血压机制。在原发性高血压中，可观察到对血管紧张素II和α-肾上腺素能受体激动剂的反应性增强。然而，在一些实验模型中，已报道有更具选择性的反应性增加。本文综述了α-肾上腺素能受体介导的血管平滑肌收缩机制，并讨论了肌醇磷酸和二酰基甘油作为第二信使的作用。高血压中血管反应性增加的确切机制仍不确定。
