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Angiotensin II type 1 autoantibody induced hypertension during pregnancy is associated with renal endothelial dysfunction

Item Type:Article
Title:Angiotensin II type 1 autoantibody induced hypertension during pregnancy is associated with renal endothelial dysfunction
Creators Name:Parrish, M.R. and Ryan, M.J. and Glover, P. and Brewer, J. and Ray, L. and Dechend, R. and Martin, J.N. and Lamarca, B.B.
Abstract:BACKGROUND: Previous investigations suggested that agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) might mediate a hypertensive response through dysregulation of the endothelin-1 system. AT1-AA induced hypertension was attenuated by the AT1 receptor and/or endothelin-1 type A receptor antagonists. OBJECTIVES: This study was undertaken to determine if AT1-AA induced hypertension was associated with renal endothelial dysfunction. METHODS: We compared the vascular reactivity of renal interlobar arteries from normal pregnant control rats and AT1-AA long-term infused pregnant rats in the presence and absence of endothelin type A (ET(A)) receptor antagonism. Renal endothelial function was tested using isolated renal interlobar arteries in a pressure myograph, which were exposed to acetylcholine or sodium nitroprusside. RESULTS: Vasodilatory responses to the endothelial-dependent agonist acetylcholine were impaired in AT1-AA rats (74 [10]%) compared with normal pregnant controls (95 [5]%, P < 0.05). In the presence of ET(A) receptor antagonism, no differences were observed between controls or the AT1-AA treated group with regard to endothelial-dependent (acetylcholine) relaxation. CONCLUSION: AT1-AA induced hypertension during pregnancy was associated with disparate renal endothelial responses to acetylcholine. The difference in renal vascular responses between AT1-AA and normal pregnant rats was abolished by ET(A) receptor blockade.
Keywords:Angiotensin, Endothelial Dysfunction, Hypertension, Pregnancy, Animals, Rats
Source:Gender Medicine
Page Range:184-188
Date:June 2011
Official Publication:https://doi.org/10.1016/j.genm.2011.04.003
PubMed:View item in PubMed

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