Sustained coronary vasoconstriction provoked by a peptidergic substance released from endothelial cells in culture.
Sustained coronary vasoconstriction provoked by a peptidergic substance released from endothelial cells in culture.
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由培养的内皮细胞释放的肽能物质引起持续的冠状血管收缩。
DOI：
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发表时间：
1986
影响因子：
3.5
通讯作者：
R. O'Brien
中科院分区：
文献类型：
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作者：
M. Gillespie;J. O. Owasoyo;I. Mcmurtry;R. O'Brien
最近的报道表明，培养的内皮细胞向培养基中释放一种（或多种）收缩动脉平滑肌分离制剂的物质[内皮源性收缩因子（EDCF）]。为了评价EDCF的冠状动脉和心脏效应，在非再循环系统中用Krebs-Henseleit溶液反灌注的离体兔心脏用无血清最低必需培养基（载体）或浓缩在最低必需培养基（EDCF）中的主动脉内皮细胞上清液的推注（100-600微升）进行挑战。EDCF，而不是其媒介物，产生剂量依赖性冠状血管收缩，不伴有左心室收缩或心率的变化。在15分钟的观察期内，收缩反应持续良好，阻力几乎没有或没有下降。硝普钠可抑制EDCF引起的血管收缩，并可逆转EDCF引起的血管收缩。无论是meclutamate或乙胺嗪影响EDCF诱导的升压反应，从而否定了花生四烯酸代谢产物的作用。EDCF诱导的冠状动脉血管收缩也不受α-肾上腺素能、组胺能或肾上腺素能受体阻断的影响。EDCF与胰蛋白酶共同孵育可明显减弱其升压作用，提示EDCF可能是一种多肽。血管紧张素或P物质的作用被排除，然而，saralasin未能影响EDCF诱导的收缩，因为P物质在灌注的兔心脏制备中是无活性的。我们的结论是一种物质（或多种物质），可能是一种肽，从培养的内皮细胞中释放，通过一种未知的机制引起持续的冠状血管收缩。
Recent reports have shown that cultured endothelial cells release into the culture medium a substance (or substances) that contracts isolated preparations of arterial smooth muscle [endothelial-derived constrictor factor (EDCF)]. To evaluate the coronary and cardiac effects of EDCF, isolated rabbit hearts retroperfused in a nonrecirculating system with Krebs-Henseleit solution were challenged with bolus injections (100-600 microliter) of either serum-free minimum essential medium (vehicle) or aortic endothelial cell supernates concentrated in minimum essential medium (EDCF). EDCF, but not its vehicle, produced dose-dependent coronary vasoconstriction unaccompanied by changes in left ventricular contraction or heart rate. The constrictor responses were remarkably well sustained with little or no decrement in resistance occurring over a 15-min observation period. Nitroprusside inhibited the development of and reversed on-going vasoconstriction evoked by EDCF. Neither meclofenamate nor diethylcarbamazine influenced EDCF-induced pressor responses, thereby negating a role for arachidonic acid metabolites. Coronary vasoconstriction induced by EDCF also was unaffected by blockade of alpha-adrenergic, histaminergic or serotonergic receptors. Incubation of EDCF with trypsin attenuated the pressor effects markedly, suggesting that EDCF may be a peptide. Roles for angiotensin or substance P were ruled out, however, as saralasin failed to influence EDCF-induced constriction and since substance P was inactive in the perfused rabbit heart preparation. We conclude that a substance (or substances), probably a peptide, released from cultured endothelial cells provokes sustained coronary vasoconstriction by an unknown mechanism.