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首页> 外文期刊>American Journal of Physiology >Are cardiovascular and sympathoadrenal effects of human 'new pressor protein' preparations attributable to human coagulation beta-FXIIa?
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Are cardiovascular and sympathoadrenal effects of human 'new pressor protein' preparations attributable to human coagulation beta-FXIIa?

机译：人类“新加压蛋白”制剂的心血管和交感肾上腺作用是否归因于人类凝血β-FXIIa？

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摘要

"New pressor protein" (NPP) derived from normal human plasma is an extra renal enzyme that shares strong sequence homology with human coagulation beta-FXIIa. Under our bioassay conditions, human NPP (10-20 microl plasma equivalent/ approximately 300 g rat iv) can raise the systolic blood pressure (SBP) by 40-50 mmHg, the diastolic blood pressure (DBP) by 15-20 mmHg, and the heart rate (HR) by 70-90 beats/min. Plasma epinephrine (of adrenal medullary origin) and norepinephrine rise by about 50- and 10-fold, respectively. Because beta-FXIIa is not normally associated with pressor properties, we endeavored to substantiate that the hypertensive effects of impure NPP preparations used in our experiments are attributable to their content of beta-FXIIa. We carried out comparisons with highly purified (>90%) commercial human beta-FXIIa and found that by gel filtration (Sephadex G-100 and G-75), NPP bioactivity appeared in the approximately 30-kDa elution zone, consistent with the molecular mass of beta-FXIIa. Retention time using fast-protein liquid chromatography anion exchange chromatography was identical. Molecular mass and comigration were confirmed by SDS-PAGE gel electrophoresis, and the recovered approximately 30-kDa protein bands yielded beta-FXIIa fragments identified by mass spectrometry. Matched doses of the NPP preparations produced dose-response curves very similar to those elicited by beta-FXIIa with respect to increments of SBP, DBP, and HR, whereas plasma catecholamine increments were generally comparable. We propose that beta-FXIIa is substantially, if not exclusively, responsible for the observed effects of our NPP preparations and that this points to a novel axis connecting the FXII coagulation cascade and the sympathoadrenal gland to other cardiovascular regulatory mechanisms.
机译：源自正常人血浆的“新加压蛋白”（NPP）是一种额外的肾脏酶，与人凝血β-FXIIa具有很强的序列同源性。在我们的生物测定条件下，人NPP（10-20微升血浆当量/约300 g大鼠静脉注射）可使收缩压（SBP）升高40-50 mmHg，舒张压（DBP）升高15-20 mmHg，并且心率（HR）降低70-90次/分钟。血浆肾上腺素（源自肾上腺髓质）和去甲肾上腺素分别升高约50倍和10倍。由于β-FXIIa通常不与升压特性相关，因此我们努力证实实验中使用的不纯NPP制剂的高血压作用可归因于其β-FXIIa的含量。我们与高度纯化（> 90％）的商业人β-FXIIa进行了比较，发现通过凝胶过滤（Sephadex G-100和G-75），NPP生物活性出现在大约30kDa的洗脱区域，与分子β-FXIIa的质量。使用快速蛋白液相色谱阴离子交换色谱的保留时间相同。通过SDS-PAGE凝胶电泳确认了分子量和迁移，并且回收的大约30kDa的蛋白条带产生了通过质谱鉴定的β-FXIIa片段。在SBP，DBP和HR的增加方面，匹配剂量的NPP制剂产生的剂量响应曲线与β-FXIIa引起的剂量响应曲线非常相似，而血浆儿茶酚胺的增加通常是可比较的。我们建议，β-FXIIa基本上（如果不是唯一的话）对我们的NPP制剂的观察到的作用负责，并且这指向一个新的轴，将FXII凝血级联和交感肾上腺与其他心血管调节机制连接起来。

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