Возбуждение альдостерона АКТГ в нормальной и гипертензивной беременности. Общее количество renin в преэклампсии, страница 15

SO: Chung-Hua-I-Hsueh-I-Chuan-Hsueh-Tsa-Chih. 1999 Feb 10; 16(1): 29-31

CP: CHINA

AB: OBJECTIVE: To establish a method for sensitive, specific and rapid detection of the angiotensin converting enzyme(ACE) genotypes and to study the relationship between the ACE gene polymorphism and preeclampsia. METHODS: Sixty patients with preeclampsia and 76 normal pregnant women as controls were investigated. A pair of primers, for the intron 16 of ACE gene was designed. A sensitive and specific method for detecting the ACE polymorphism of the insertion/deletion was established. Determined by polymerase chain reaction (PCR),a 490bp(I) and 190bp(D) PCR product was identified,corresponding to the PCR amplification of the allele with or without the insertion. RESULTS: The subjects were classified, according to the presence or absence of a 287bp insertion in intron 16 of the ACE gene, as II, DD, or heterozygotes for deletion/insertion (DI).The frequency of allele gene (0.75) and the percentage of the ACE DD genotype (65%) in the preeclampsia group were significantly higher as compared with the frequency 10.308 and the percentage (10.5%) in the control group respectively. CONCLUSION: Genotype II of ACE is a marker for reduced risk for preeclampsia and DD is a risk gene.

: Отрабатывать метод для чувствительного, определенного и быстрого обнаружения angiotensin преобразование фермента генотипы (ТУЗА) и изучать отношения между полиморфизмом гена ТУЗА и преэклампсией. МЕТОДЫ: Шестьдесят пациентов с преэклампсией и 76 нормальными беременными женщинами как контрольные группы были исследованы. Пара инициаторов, для intron 16 из гена ТУЗА была разработана(предназначена). Чувствительный и определенный метод чтобы обнаруживать полиморфизм ТУЗА вставки/стирания был отработан(установлен). Определенный полимеразной реакцией цепи (PCR), 490bp (I) и 190bp (D) PCR продукт был идентифицирован, соответствуя PCR усилению allele с или без вставки. РЕЗУЛЬТАТЫ: субъекты были отнесены(классифицированы), согласно наличию или отсутствию 287bp вставка в intron 16 из гена ТУЗА, как II, DD, или heterozygotes для стирания/вставки (ДИ) .T Частота allele гена (0.75) и процента от ТУЗА DD генотип (65 %) в группе преэклампсии была значительно выше по сравнению с частотой 10.308 и процентом (10.5 %) в контрольной группе соответственно. ЗАКЛЮЧЕНИЕ: Генотип II из ТУЗА являются маркером для сниженного риска для преэклампсии и DD - ген риска.

TI: Patients with preeclampsia develop agonistic autoantibodies against the angiotensin AT1 receptor.

Пациенты с преэклампсией развивают agonistic автоантитела против angiotensin AT1 рецептор.

AU: Wallukat-G; Homuth-V; Fischer-T; Lindschau-C; Horstkamp-B; Jupner-A; Baur-E; Nissen-E; Vetter-K; Neichel-D; Dudenhausen-JW; Haller-H; Luft-FC

AD: Franz Volhard Clinic at the Max Delbruck Center for Molecular Medicine, Humboldt University of Berlin, 13122 Berlin, Germany.

SO: J-Clin-Invest. 1999 Apr; 103(7): 945-52

CP: UNITED-STATES

AB: Immune mechanisms and the renin-angiotensin system are implicated in preeclampsia. We investigated 25 preeclamptic patients and compared them with 12 normotensive pregnant women and 10 pregnant patients with essential hypertension. Antibodies were detected by the chronotropic responses to AT1 receptor-mediated stimulation of cultured neonatal rat cardiomyocytes coupled with receptor-specific antagonists. Immunoglobulin from all preeclamptic patients stimulated the AT1 receptor, whereas immunoglobulin from controls had no effect. The increased autoimmune activity decreased after delivery. Affinity-column purification and anti-human IgG and IgM antibody exposure implicated an IgG antibody directed at the AT1 receptor. Peptides corresponding to sites on the AT1 receptor's second extracellular loop abolished the stimulatory effect. Western blotting with purified patient IgG and a commercially obtained AT1 receptor antibody produced bands of identical molecular weight. Furthermore, confocal microscopy of vascular smooth muscle cells showed colocalization of purified patient IgG and AT1 receptor antibody. The protein kinase C (PKC) inhibitor calphostin C prevented the stimulatory effect. Our results suggest that preeclamptic patients develop stimulatory autoantibodies against the second extracellular AT1 receptor loop. The effect appears to be PKC-mediated. These novel autoantibodies may participate in the angiotensin II-induced vascular lesions in these patients.