Plasma catecholamine modulation of alpha 2 adrenoreceptor agonist affinity and sensitivity in normotensive and hypertensive human platelets.

Plasma catecholamine modulation of alpha 2 adrenoreceptor agonist affinity and sensitivity in normotensive and hypertensive human platelets.
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血浆儿茶酚胺调节正常血压和高血压人血小板中α2肾上腺素受体激动剂亲和力和敏感性。

DOI:
10.1172/jci112452
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发表时间:
1986
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
Robertson,D
Robertson,D
中科院分区:
--
文献类型:
--
作者:
Hollister,AS;Onrot,J;Lonce,S;Nadeau,JH;Robertson,D

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在血浆儿茶酚胺生理性增加前后,我们测量了正常血压和高血压患者完整血小板上的α2-肾上腺素受体密度以及对激动剂的亲和力和敏感性。在血压正常的人中,体位引起的血浆儿茶酚胺的升高与α2肾上腺素受体激动剂亲和力降低和高亲和力状态受体减少相关。L-肾上腺素对血小板聚集和腺苷环化酶抑制作用也明显降低。高血压患者在直立状态下血浆儿茶酚胺水平也有类似的升高,但受体亲和力或敏感性没有变化。在这些研究中,血小板α2-肾上腺素受体数量没有发生变化。体外与L肾上腺素孵育发现,高血压患者的血小板脱敏慢于正常血压患者。在不同温度和不同钠浓度下的结合研究发现,正常血压组和高血压组之间没有热力学或钠依赖性差异。这些研究表明,高血压患者的血小板在生理浓度的激动剂脱敏α2-肾上腺素受体的能力方面存在缺陷。
We measured alpha 2-adrenoreceptor density as well as affinity for and sensitivity to agonist on intact platelets of normotensive and hypertensive subjects before and after physiological increases in plasma catecholamines. In normotensives, posture-induced rises in plasma catecholamines correlated with reduced alpha 2-adrenoreceptor agonist affinity and fewer high affinity state receptors. Platelet aggregation and inhibition of adenylate cyclase by L-epinephrine also was reduced. Hypertensive subjects had similar rises in plasma catecholamines with upright posture, but showed no change in receptor affinity or sensitivity. No change in platelet alpha 2-adrenoreceptor number occurred in these studies. In vitro incubation with L-epinephrine revealed that platelets from hypertensives had slower desensitization than those from normotensives. Binding studies at different temperatures and with varying sodium concentrations found no thermodynamic or sodium-dependent differences between normotensive and hypertensive groups. These studies demonstrate that platelets from hypertensive subjects exhibit a defect in the ability of physiological concentrations of agonist to desensitize the alpha 2-adrenoreceptor.