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2016 ; 68
(5
): 1308-1313
Nephropedia Template TP
gab.com Text
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Twit Text #
English Wikipedia
Agonistic Autoantibodies to the Angiotensin II Type 1 Receptor Enhance
Angiotensin II-Induced Renal Vascular Sensitivity and Reduce Renal Function
During Pregnancy
#MMPMID27698062
Cunningham MW Jr
; Williams JM
; Amaral L
; Usry N
; Wallukat G
; Dechend R
; LaMarca B
Hypertension
2016[Nov]; 68
(5
): 1308-1313
PMID27698062
show ga
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.
|*Pregnancy, Animal
[MESH]
|Analysis of Variance
[MESH]
|Angiotensin II Type 1 Receptor Blockers/pharmacology
[MESH]