Roma Gurusankar, Prem Kumarathasan, Anusha Saravanamuthu, Errol M Thomson, Renaud Vincent
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引用次数: 5
摘要
尽管唾液内皮素正在成为有价值的无创心血管生物标志物,但关于唾液和血浆中同种异构体之间关系的报道仍然很少。我们同时测量了唾液和血浆样本中的内皮素(n = 30名男性;年龄18-63岁)。结果显示,唾液和血浆各亚型之间存在显著正相关:大内皮素-1 (BET-1)为0.55±0.27比3.35±1.28 pmol/mL;r = 0.38, p = 0.041),内皮素-1 (ET-1, 0.52±0.21比3.45±1.28 pmol/mL;r = 0.53, p = 0.003),内皮素-2 (ET-2, 0.21±0.07 vs 1.63±0.66 pmol/mL;r = 0.51, p = 0.004),内皮素-3 (ET-3, 0.39±0.19 vs 2.32±1.44 pmol/mL;R = 0.75, p < 0.001)。血浆和唾液中ET-1、ET-1和ET-3的相关性均为正(p < 0.05),而ET-2与血浆和唾液中其他亚型的相关性均不显著。对于所有同种异构体,个体之间的浓度平均相差5倍(90 /10百分位数);血浆内皮素水平高的个体通常唾液内皮素水平也高。我们的研究结果表明,唾液ET异构体谱描绘了血浆谱,并支持ET-1和ET-3协调调节的观点,但ET-2的调节途径不同。
Correlation between Saliva and Plasma Levels of Endothelin Isoforms ET-1, ET-2, and ET-3.
Although saliva endothelins are emerging as valuable noninvasive cardiovascular biomarkers, reports on the relationship between isoforms in saliva and plasma remain scarce. We measured endothelins in concurrent saliva and plasma samples (n = 30 males; age 18-63) by HPLC-fluorescence. Results revealed statistically significant positive correlations among all isoforms between saliva and plasma: big endothelin-1 (BET-1, 0.55 ± 0.27 versus 3.35 ± 1.28 pmol/mL; r = 0.38, p = 0.041), endothelin-1 (ET-1, 0.52 ± 0.21 versus 3.45 ± 1.28 pmol/mL; r = 0.53, p = 0.003), endothelin-2 (ET-2, 0.21 ± 0.07 versus 1.63 ± 0.66 pmol/mL; r = 0.51, p = 0.004), and endothelin-3 (ET-3, 0.39 ± 0.19 versus 2.32 ± 1.44 pmol/mL; r = 0.75, p < 0.001). Correlations of BET-1, ET-1, and ET-3 within each compartment were positive in both plasma (p < 0.05) and saliva (p ≤ 0.1), whereas ET-2 was not significantly correlated with other isoforms in either plasma or saliva. For all isoforms, concentrations varied on average fivefold between individuals (90th/10th percentiles); individuals with high plasma endothelin levels generally had high saliva endothelin levels. Our results reveal that salivary ET isoform profiles portray the plasmatic profiles and support the view of coordinated regulation of ET-1 and ET-3, but distinct regulatory pathways for ET-2.