Koch G
Acta Med Scand Suppl. 1982;665:87-92. doi: 10.1111/j.0954-6820.1982.tb00414.x.
Increased peripheral vascular resistance is the cause of elevated blood pressure in most forms of systemic hypertension. Both structural changes in response to increased wall stress and functional alterations in vascular smooth muscle itself appear to contribute to the elevated resistance. As mediators of the vasoconstrictor responses, alpha-adrenoceptors apparently play an important if not predominant role in the initiation and/or maintenance of high resistance and pressure. In contrast to beta-receptor blockade alone, combined alpha-beta-receptor blockade lowers blood pressure predominantly by alpha-receptor-mediated reduction of the systemic vascular resistance, both when induced acutely and, in particular, during long-term administration. Cardiac output is maintained at pretreatment level, as is left ventricular filling pressure. Since a well-balanced blockade of both alpha- and beta-receptors counteracts the pathophysiological changes causing and/or maintaining hypertension and tends to restore cardiovascular dynamics towards normal, combined alpha-beta-receptor blockade appears at present to be one of the most logical and rational therapeutic approaches to hypertension.
在大多数类型的系统性高血压中，外周血管阻力增加是血压升高的原因。对增加的壁应力的结构变化以及血管平滑肌本身的功能改变似乎都导致了阻力升高。作为血管收缩反应的介质，α-肾上腺素受体显然在高阻力和高血压的起始和/或维持中发挥着重要作用，即便不是主导作用。与单独的β受体阻滞剂相比，联合α-β受体阻滞剂降低血压主要是通过α受体介导的全身血管阻力降低，无论是急性诱导还是特别是在长期给药期间。心输出量维持在治疗前水平，左心室充盈压也是如此。由于对α和β受体的平衡阻断可抵消导致和/或维持高血压的病理生理变化，并倾向于使心血管动力学恢复正常，联合α-β受体阻滞剂目前似乎是治疗高血压最合理、最合乎逻辑的治疗方法之一。
