可乐定引起的中枢α-激活降低原发性高血压患者的β-内啡肽血浆水平。
Central alpha-activation by clonidine reduces plasma level of beta-endorphin in patients with essential hypertension.
作者信息
Yasunari K, Kanayama Y, Kohno M, Murakawa K, Kawarabayashi T, Takeda T, Kotsugai N, Sato K
出版信息
Life Sci. 1985 Oct 21;37(16):1461-7. doi: 10.1016/0024-3205(85)90176-6.
Whether peripheral beta-endorphin contributes to the antihypertensive action of clonidine was examined by measuring plasma levels of beta-endorphin-like immunoreactivity (beta EpLI) after acute administration of clonidine in patients with essential hypertension. Administration of clonidine (0.225 mg) in one dose significantly lowered blood pressure, decreased heart rate and reduced the plasma level of beta EpLI and ACTH, while the placebo had no effect on blood pressure, heart rate or plasma level of beta EpLI suggesting that peripheral beta-endorphin does not play a major role in the antihypertensive action of acute clonidine administration.
通过测量原发性高血压患者急性服用可乐定后血浆中β-内啡肽样免疫反应性（βEpLI）水平，研究外周β-内啡肽是否有助于可乐定的降压作用。单次服用可乐定（0.225mg）可显著降低血压、减慢心率，并降低血浆βEpLI和促肾上腺皮质激素（ACTH）水平，而安慰剂对血压、心率或血浆βEpLI水平无影响，这表明外周β-内啡肽在急性服用可乐定的降压作用中不起主要作用。
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