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钙通道阻滞剂维拉帕米和地尔硫䓬是血管加压素诱导的人血小板活化的抑制剂。

Calcium-channel blocking agents verapamil and diltiazem are inhibitors of vasopressin-induced human platelet activation.

作者信息

Anfossi G, Mularoni E, Massucco P, Cavalot F, Burzacca S, Mattiello L, Trovati M

机构信息

Department of Clinical and Biological Sciences, University of Turin, Ospedale S. Luigi Gonzaga, Orbassano, Torino, Italy.

出版信息

Clin Exp Pharmacol Physiol. 1991 Nov;18(11):767-73. doi: 10.1111/j.1440-1681.1991.tb01395.x.

DOI:10.1111/j.1440-1681.1991.tb01395.x
PMID:1782723
Abstract
  1. This study investigated the influences of calcium-channel blocking agents verapamil and diltiazem on platelet responses induced by arginine vasopressin (AVP) and lysine vasopressin (LVP). 2. The substances inhibited platelet aggregation induced by both low and high AVP concentrations, LVP and adrenaline plus AVP. IC50 values of each drug are lower than those determined for ADP- and collagen-elicited aggregation. Verapamil and diltiazem also decreased AVP-induced thromboxane B2 synthesis. 3. Other series of experiments showed that the addition of ethyleneglycol-bis-(beta-amino-ethyl ether) N, N'-tetra-acetic acid to platelet-rich plasma samples also prevented the platelet response to vasopressin polypeptides. 4. Our data provide evidence that the effects of verapamil and diltiazem on vasopressin-induced platelet responses may be directly related to inhibition of extracellular calcium entry.
摘要
  1. 本研究调查了钙通道阻滞剂维拉帕米和地尔硫䓬对精氨酸加压素(AVP)和赖氨酸加压素(LVP)诱导的血小板反应的影响。2. 这些物质抑制了低浓度和高浓度AVP、LVP以及肾上腺素加AVP诱导的血小板聚集。每种药物的IC50值均低于ADP和胶原诱导聚集所测定的值。维拉帕米和地尔硫䓬也降低了AVP诱导的血栓素B2合成。3. 其他系列实验表明,向富含血小板的血浆样本中添加乙二醇双(β-氨基乙醚)N,N'-四乙酸也可防止血小板对加压素多肽的反应。4. 我们的数据提供了证据,表明维拉帕米和地尔硫䓬对加压素诱导的血小板反应的影响可能与抑制细胞外钙内流直接相关。

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Calcium-channel blocking agents verapamil and diltiazem are inhibitors of vasopressin-induced human platelet activation.钙通道阻滞剂维拉帕米和地尔硫䓬是血管加压素诱导的人血小板活化的抑制剂。
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