Angiotensin-(1-7) in normal and preeclamptic pregnancy
Angiotensin-(1-7) in normal and preeclamptic pregnancy
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DOI：
10.1385/endo:18:3:239
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发表时间：
2002-08-01
期刊：
影响因子：
3.7
通讯作者：
Brosnihan, KB
中科院分区：
文献类型：
--
作者：
Merrill, DC;Karoly, M;Brosnihan, KB
血管紧张素-(1-7) (Ang-[1-7]) 是肾素-血管紧张素系统的生物活性成分，具有降压、血管舒张和抗高血压作用。在正常妊娠中，我们质疑已知的血浆血管紧张素 II (Ang II) 升高是否会被血浆 Ang-(1-7) 升高所抵消，以及 Ang-(1-7) 水平在先兆子痫中是否降低，从而可能是导致高血压发生的一个因素。未产子先兆子痫受试者、妊娠晚期血压正常的怀孕受试者和非怀孕组均纳入研究（n = 15/组）。先兆子痫受试者既往没有高血压或肾脏、结缔组织或代谢疾病史，但在分娩时有明显的高血压（159+/-3/98+/-3mmHg）和大于或等于3+蛋白尿。正常妊娠时血浆 Ang-(1-7) 增加 51% (p < 0.05)。正常妊娠时血浆血管紧张素 I、血管紧张素 II 和肾素活性也显着升高。与正常妊娠受试者相比，先兆子痫受试者的 Ang-(1-7) 显着降低 (p < 0.01)。与正常妊娠受试者相比，先兆子痫受试者的肾素-血管紧张素-醛固酮系统的所有其他成分（血清血管紧张素转换酶除外）均减少；与非妊娠受试者相比，只有先兆子痫患者的血浆血管紧张素 II 仍然升高。这些研究首次证明，与非妊娠受试者相比，正常妊娠受试者的血浆 Ang-(1-7) 升高，而与正常妊娠受试者相比，先兆子痫受试者的血浆 Ang-(1-7) 降低。在先兆子痫中，在 Ang II 升高的情况下血浆 Ang-(1-7) 降低与高血压的发展一致。
Angiotensin-(1-7) (Ang-[1-7]) is a bioactive component of the renin-angiotensin system, which has depressor, vasodilatory, and anti hypertensive actions. In normal Pregnancy, we questioned whether the known rise in plasma angiotensin II (Ang II) is counterbalanced by an increase in plasma Ang-(1-7) and whether Ang-(1-7) levels are decreased in preeclampsia and may thus be a factor involved in the development of hypertension. Nulliparous preeclamptic subjects, third-trimester normotensive pregnant subjects, and a nonpregnant group were enrolled (n = 15/group). Preeclamptic subjects had no previous history of hypertension or renal, connective-tissue, or metabolic disease, but at the time of delivery had significant hypertension (159 +/- 3/98 +/- 3 mmHg) and greater than or equal to3+ proteinuria. Plasma Ang-(1-7) was increased by 51 % in normal pregnancy (p < 0.05). Plasma Ang I, Ang II, and renin activity were also significantly elevated in normal pregnancy. In preeclamptic subjects, Ang-(1-7) was significantly decreased (p < 0.01) compared with normal pregnant subjects. All other components of the renin-angiotensin-aldosterone system, except serum angiotensin-converting enzyme, were reduced in preeclamptic subjects compared with normal pregnant subjects; only plasma Ang II remained elevated in preeclamptic compared with nonpregnant subjects. These studies demonstrate, for the first time, increased plasma Ang-(1-7) in normal pregnant subjects compared with nonpregnant subjects and decreased Ang-(1-7) in preeclamptic subjects compared with normal pregnant subjects. In preeclampsia the decreased plasma Ang-(1-7) in the presence of elevated Ang II is consistent with the development of hypertension.