Comparative study of platelet angiotensin II binding and the angiotensin II sensitivity test as predictors of pregnancy-induced hypertension

1992 ◽  
Vol 83 (1) ◽  
pp. 89-95 ◽  
Author(s):  
Philip N. Baker ◽  
Fiona Broughton Pipkin ◽  
E. Malcolm Symonds

1. Platelet angiotensin II binding was measured in 34 primigravid women (between 28 and 32 weeks gestation), in whom the pressor response to infused angiotensin II was also determined. 2. There was a significant correlation between the platelet angiotensin II binding and the slope of the curve relating the diastolic pressor response to infused angiotensin II (P<0.01), suggesting that co-linearity between the two techniques exists and supporting the use of platelet angiotensin II binding as a model of vascular smooth muscle pressor responsiveness. 3. Ten of the 34 women subsequently developed pregnancy-induced hypertension. Platelet angiotensin II binding in the patients who subsequently developed pregnancy-induced hypertension was sixfold higher than in the patients who remained normotensive (P < 0.001). There were, however, no significant differences between the groups in any of the parameters derived from the angiotensin II infusion experiments. 4. The use of platelet angiotensin II binding alone in predicting the outcome of the pregnancies, as assessed using discriminant analysis, was more successful than when any of the infusion parameters were used, with 77% of patients being correctly classified.

Circulation ◽  
2005 ◽  
Vol 112 (17) ◽  
pp. 2668-2676 ◽  
Author(s):  
Anna Dikalova ◽  
Roza Clempus ◽  
Bernard Lassègue ◽  
Guangjie Cheng ◽  
James McCoy ◽  
...  

Pharmacology ◽  
2019 ◽  
Vol 104 (5-6) ◽  
pp. 226-234 ◽  
Author(s):  
Yunfeng Zhao ◽  
Kun Liu ◽  
Delu Yin ◽  
Zhaoheng Lin

Introduction: Angiotensin II (AngII) induces hypertension and pathophysiological vascular thickening and atherosclerosis. This study aims to validate the effects of Angiopoietin-like 7 (ANGPTL7) in AngII-induced hypertension. Methods: ANGPTL7 in blood samples were determined by quantitative real-time polymerase chain reaction. AngII-induced cell growth were detected by CCK-8. Cell cycle arrest and cell apoptosis by downregulation of ANGPTL7 were detected by flow cytometric assay. AngII-induced inflammation was evaluated by Western blotting and ELISA. Results: ANGPTL7 was highly expressed in patients with hypertension. AngII promoted cell viability and the expression level of ANGPTL7 in vascular smooth muscle cells (VSMC). Downregulation of ANGPTL7 inhibited AngII-induced cell proliferation and cell inflammation. Moreover, ANGPTL7 expression decreases also promoted cell apoptosis. Conclusions: Downregulation of ANGPTL7 reversed AngII-induced cell proliferation and cell inflammation and promoted apoptosis in AngII-induced VSMC cells. Therefore, ANGPTL7 can be a potential target in AngII-induced hypertension.


1975 ◽  
Vol 228 (1) ◽  
pp. 110-114 ◽  
Author(s):  
EL Bravo ◽  
MC Khosla ◽  
FM Bumpus

Angiotensin II receptors in vascular smooth muscle and adrenal cortex have been characterized in the dog. The evidence was derived chiefly from experiments that assessed the ability of a structural analog of angiotensin II, [Sar1, Ile8] AII, to antagonize the effects of exogenously administered angiotensin II on arterial pressure and aldosterone secretion. [Sar1, Ile8] AII is a potent and specific blocker of the pressor response to angiotensinII; in the adrenal cortex, it is a much less effective inhibitor of aldosterone biosynthesis. These results indicate differences in the receptor sites for angiotensin II in vascular smooth muscle and adrenal cortex. Further, they raise the possibility that angiotensin II stimulates aldosterone secretion by mechanisms other than have already been proposed.


2011 ◽  
Vol 91 (1) ◽  
pp. 171-179 ◽  
Author(s):  
Annet Kirabo ◽  
Patrick N. Kearns ◽  
Yagna P. Jarajapu ◽  
Jennifer M. Sasser ◽  
Suk Paul Oh ◽  
...  

Author(s):  
Jessica L. Fry ◽  
Yasunaga Shiraishi ◽  
Raphaël Turcotte ◽  
Xunjie Yu ◽  
Yuan Z. Gao ◽  
...  

1999 ◽  
Vol 276 (2) ◽  
pp. R530-R538 ◽  
Author(s):  
Janice K. Crews ◽  
Jacqueline Novak ◽  
Joey P. Granger ◽  
Raouf A. Khalil

We have previously found that the vascular responsiveness to α1-adrenergic agonists is reduced in pregnant rats and enhanced in a rat model of pregnancy-induced hypertension produced by chronic treatment of pregnant rats with the nitric oxide (NO) synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME). The purpose of this study was to investigate whether the observed changes in vascular reactivity during normal pregnancy and during pregnancy-induced hypertension reflect changes in the mechanisms of Ca2+ entry into vascular smooth muscle.45Ca2+influx and active stress during α1-adrenergic stimulation by phenylephrine and membrane depolarization by 96 mM KCl were measured in deendothelialized aortic strips isolated from virgin and pregnant Sprague-Dawley rats untreated or treated with 1 mg/dayl-NAME for 4–6 days and incubated in Krebs solution containing increasing concentrations of extracellular Ca2+([Ca2+]e). In all groups of rats, both phenylephrine and 96 mM KCl caused [Ca2+]e-dependent increases in active stress and45Ca2+influx. The phenylephrine- and 96 mM KCl-induced active stress and Ca2+ influx were significantly reduced in pregnant rats but significantly enhanced in pregnant rats treated with l-NAME. The phenylephrine-induced Ca2+influx-stress relationship was significantly greater than that induced by 96 mM KCl in pregnant rats treated withl-NAME. The phenylephrine-induced Ca2+influx-stress relationship was reduced in pregnant rats but enhanced in pregnant rats treated withl-NAME. Chronic treatment withl-NAME had minimal effect on active stress, Ca2+ influx, and the Ca2+ influx-stress relationship in virgin rats. These results provide evidence that the mechanisms of Ca2+ entry into vascular smooth muscle are inhibited during pregnancy but enhanced during inhibition of NO synthesis in late pregnancy. The enhancement of the phenylephrine-induced Ca2+influx-stress relationship in pregnant rats treated withl-NAME suggests activation of other contractile mechanisms in addition to stimulation of Ca2+ entry. These mechanisms appear to be inhibited during normal pregnancy.


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