The results illustrate a new paradigm for the developmental origins of hypertension and imply that GRK4 and dopamine D<sub>1</sub> receptor may be crucial determinants for the maternal hypertension.
We evaluated the plasmatic levels of NO metabolites, cyclic guanosine monophosphate (cGMP), oxidative stress and myeloperoxidase, which are involved in endothelial dysfunction during hypertension in pregnancy.
We have previously described improvement in maternal hypertension and fetal growth restriction in this model after treatment with the anti-inflammatory cyclooxygenase-2 (Cox2) specific inhibitor celecoxib.
The results suggest that maternal hypertension induces a sex-specific sensitization of ANG II-induced hypertension and mRNA expression of brain RAAS and NADPH oxidase in offspring.
The results suggest that maternal hypertension induces a sex-specific sensitization of ANG II-induced hypertension and mRNA expression of brain RAAS and NADPH oxidase in offspring.
The results suggest that maternal hypertension induces a sex-specific sensitization of ANG II-induced hypertension and mRNA expression of brain RAAS and NADPH oxidase in offspring.
Multivariable adjusted analyses showed an inverse relationship between SBP with depression (coefficient = -0.10; P = 0.012) and anxiety (after excluding two outliers with SBP > 156 mmHg, coefficient = -0.13; P = 0.018) scores, independent of sex, BMI, female hormonal contraceptive use, alcohol consumption, birth weight and maternal hypertension in pregnancy.
The data suggest that targeting MMP-1 and MMP-7 and their upstream modulators, such as TNF-α, could provide a new approach in the management of hypertension in pregnancy and preeclampsia.
Multivariable adjusted analyses showed an inverse relationship between SBP with depression (coefficient = -0.10; P = 0.012) and anxiety (after excluding two outliers with SBP > 156 mmHg, coefficient = -0.13; P = 0.018) scores, independent of sex, BMI, female hormonal contraceptive use, alcohol consumption, birth weight and maternal hypertension in pregnancy.
Multivariable adjusted analyses showed an inverse relationship between SBP with depression (coefficient = -0.10; P = 0.012) and anxiety (after excluding two outliers with SBP > 156 mmHg, coefficient = -0.13; P = 0.018) scores, independent of sex, BMI, female hormonal contraceptive use, alcohol consumption, birth weight and maternal hypertension in pregnancy.
Thus, the increased BP and decreased pup weight in placental ischemia model of HTN-Preg are associated with a decrease in MMP-9 homodimer and an increase in MMP-9/TIMP-1 complex in placenta, uterus, and uterine artery, which together would cause a net decrease in MMP-9 activity and reduce uteroplacental and vascular remodeling in the setting of HTN-Preg and IUGR.
The results did not support the hypothesis that hypertension in pregnancy is a trait associated with polymorphic variants of the HTR2A and SLC6A4 or that they have a role in the predisposition to hypertensive disorders in pregnancy.
The results did not support the hypothesis that hypertension in pregnancy is a trait associated with polymorphic variants of the HTR2A and SLC6A4 or that they have a role in the predisposition to hypertensive disorders in pregnancy.
Gene-environment interactions were identified for rs523349 in SRD5A2 with estrogen exposure and maternal hypertension or preeclampsia, as well as for rs11119982 in ATF3 with exposure to cytokines.
Gene-environment interactions were identified for rs523349 in SRD5A2 with estrogen exposure and maternal hypertension or preeclampsia, as well as for rs11119982 in ATF3 with exposure to cytokines.
T235 of AGT, C1166 of AT1 and Asp298 of NOS3 were respectively associated with HP, although no significant associations were found between the common genetic variants and HP in ACE, FV, MTHFR, B3AR, TNF-A, PAI-1, GSTP1, mEH, and LPL.
T235 of AGT, C1166 of AT1 and Asp298 of NOS3 were respectively associated with HP, although no significant associations were found between the common genetic variants and HP in ACE, FV, MTHFR, B3AR, TNF-A, PAI-1, GSTP1, mEH, and LPL.
These results suggest that this variant of the GSTP1 may play a role in the manifestation of HP together with other independently and/or synergistically acting factors, particularly in primiparous pregnancy.