Effects on the renin-angiotensin system of agents acting at central and peripheral adrenergic receptors.
Effects on the renin-angiotensin system of agents acting at central and peripheral adrenergic receptors.
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作用于中枢和外周肾上腺素能受体的药物对肾素-血管紧张素系统的影响。
DOI：
10.1378/chest.83.2_supplement.374
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发表时间：
1983
期刊：
影响因子：
9.6
通讯作者：
F. Hubbell
中科院分区：
文献类型：
--
作者：
M. Weber;J. Drayer;F. Hubbell
虽然可乐定的主要作用与其中枢介导的交感神经活性抑制有关，但其对肾素轴的抑制也可能有助于其抗高血压作用。在临床研究中心研究的原发性高血压患者中，可乐定诱导的舒张压和血浆肾素活性（PRA）降低在治疗一天后密切相关，但此后则不相关。此外，在治疗的第一天，高肾素患者经历了显着更大的血压下降比低肾素患者，但随后的血压下降是相等的两组，证实可乐定的交感神经抑制作用可能是独立的肾素-血管紧张素系统。然而，可乐定治疗的反应者比无反应者表现出更大的醛固酮排泄率下降。在门诊研究中，与普萘洛尔相比，可乐定降低醛固酮水平的程度与普萘洛尔相同，尽管对PRA的抑制作用明显较弱。事实上，在与哌唑嗪的进一步比较研究中，在这两种药物都没有降低肾素水平的情况下，可乐定显著降低了醛固酮的排泄。因此，可乐定似乎对肾素-醛固酮轴有两种独立的作用：主要在高肾素患者中的早期抗肾素作用和对醛固酮的长期抑制作用。后一种作用可能与肾素的变化无关，可能反映了通过中枢机制介导的对醛固酮释放的影响。
Although the principal actions of clonidine are linked to its centrally mediated suppression of sympathetic activity, its inhibition of the renin axis also may contribute to its antihypertensive effects. In patients with essential hypertension studied in a clinical research center, clonidine-induced decreases in diastolic blood pressure and in plasma renin activity (PRA) correlated closely after one day of treatment, but not thereafter. Moreover, high-renin patients experienced significantly greater blood pressure decrements than low-renin patients during the first day of treatment, but subsequent blood pressure decreases were equal in the two groups, confirming that the sympathoinhibitory action of clonidine is probably independent of the renin-angiotensin system. However, responders to clonidine treatment exhibited significantly greater decrements in aldosterone excretion rate than nonresponders. When compared with propranolol in an outpatient study, clonidine reduced aldosterone levels to the same extent as propranolol despite a significantly weaker inhibitory effect on PRA. Indeed, in a further comparative study with prazosin, during which neither agent decreased renin levels, clonidine significantly lowered aldosterone excretion. Thus, clonidine appears to have two separate actions on the renin-aldosterone axis: an early antirenin action primarily in high-renin patients, and a longer-term suppressive effect on aldosterone. This latter action is possibly independent of changes in renin, and perhaps reflects an effect on aldosterone release mediated through central mechanisms.