Vascular contractile potency of endothelin-1 is increased in the presence of monocytes or macrophages.
Vascular contractile potency of endothelin-1 is increased in the presence of monocytes or macrophages.
复制标题
当单核细胞或巨噬细胞存在时，内皮素-1 的血管收缩能力会增强。
DOI：
10.1152/ajpheart.1994.266.4.h1620
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Malik,AB
中科院分区：
文献类型：
--
作者：
Magazine,HI;Andersen,TT;Bruner,CA;Malik,AB
炎症细胞的积累和对血管活性介质的反应性改变是动脉粥样硬化血管中常见的事件。我们研究了单核细胞对内皮素-1 （ET-1）诱导的豚鼠颈动脉条收缩的影响。在人外周血单核细胞、豚鼠肺泡巨噬细胞（M phi）和人单核细胞系THP-1存在的情况下，ET-1的血管收缩力明显增强。检测到125i标记的ET-1与这些细胞的特异性结合，Scatchard分析表明解离常数值约为1 nM。相比之下，人类单核细胞系U-937未能结合125I-ET-1，也没有改变ET-1的效力，这表明单核细胞提高ET-1效力的能力需要ET受体的表达。BQ-123选择性抑制ET-1与血管平滑肌的结合，一种不抑制ET-1与单核细胞结合的ETA受体拮抗剂，导致血管收缩完全抑制。这些数据表明，et -1诱导的血管收缩可能通过单核细胞内皮素受体的刺激而增加。
Accumulation of inflammatory cells and altered responsiveness to vasoactive mediators are commonly observed events in atherosclerotic vessels. We studied the effect of monocytic cells on endothelin-1 (ET-1)-induced contraction of strips of guinea pig carotid artery. The vascular contractile potency of ET-1 was increased markedly in the presence of human peripheral blood monocytes, guinea pig alveolar macrophages (M phi), and the human monocytic cell line, THP-1. Specific binding of 125I-labeled ET-1 to these cells was detected, and Scatchard analysis indicated a dissociation constant value of approximately 1 nM. In contrast, the human monocytic cell line, U-937, failed to bind 125I-ET-1 and did not alter ET-1 potency, suggesting that the ability of monocytic cells to increase ET-1 potency requires expression of ET receptors. Selective inhibition of ET-1 binding to vascular smooth muscle with BQ-123, an ETA receptor antagonist that does not inhibit ET-1 binding to monocytes, resulted in complete inhibition of vascular contraction. These data indicate that ET-1-induced vasoconstriction may be increased by monocytic cells via stimulation of monocyte endothelin receptors.