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| Item Type: | Article |
|---|---|
| Title: | Agonistic autoantibodies to the angiotensin II type 1 receptor enhance angiotensin II-induced renal vascular sensitivity and reduce renal function during pregnancy |
| Creators Name: | Cunningham, M.W., Williams, J.M., Amaral, L., Usry, N., Wallukat, G., Dechend, R. and LaMarca, B. |
| Abstract: | Preeclamptic women produce agonistic autoantibodies to the angiotensin II type 1 receptor (AT1-AA) and exhibit increased blood pressure (mean arterial pressure), vascular sensitivity to angiotensin II (ANG II), and display a decrease in renal function. The objective of this study was to examine the renal hemodynamic changes during pregnancy in the presence of AT1-AAs with or without a slow pressor dose of ANG II. In this study, mean arterial pressure was elevated in all pregnant rats treated with ANG II with or without AT1-AA. Glomerular filtration rate was reduced from 1.90+/-0.16 mL/min in normal pregnant (NP) to 1.20+/-0.08 in ANG II+AT1-AA rats. Renal blood flow was decreased in ANG II+AT1-AA versus NP rats to 7.4+/-1.09 versus 15.4+/-1.75 mL/min. Renal vascular resistance was drastically increased between ANG II+AT1-AA versus NP rats (18.4+/-2.91 versus 6.4+/-0.77 mm Hg/mL per minute). Isoprostane excretion was increased by 3.5-fold in ANG II+AT1-AA versus NP (1160+/-321 versus 323+/-52 pg/mL). In conclusion, ANG II and AT1-AA together significantly decrease glomerular filtration rate by 37% and renal blood flow by 50% and caused a 3-fold increase in renal vascular resistance and isoprostane levels versus NP rats. These data indicate the importance of AT1-AAs to enhance ANG II-induced renal vasoconstriction and reduce renal function as mechanisms to cause hypertension as observed during preeclampsia. |
| Keywords: | Angiotensin II, Autoantibodies, Hypertension, Preeclampsia, Pregnancy, Animals, Rats |
| Source: | Hypertension |
| ISSN: | 0194-911X |
| Publisher: | American Heart Association |
| Volume: | 68 |
| Number: | 5 |
| Page Range: | 1308-1313 |
| Date: | November 2016 |
| Additional Information: | Copyright © 2016 American Heart Association, Inc. |
| Official Publication: | https://doi.org/10.1161/HYPERTENSIONAHA.116.07971 |
| External Fulltext: | View full text on PubMed Central |
| PubMed: | View item in PubMed |
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