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.
A multivariate analysis with "AC+CC genotype of AT1" and "TT genotype of AGT" revealed that these were independently associated with primiparous severe HP.
By dividing the subjects into two subgroups--those who possessed "the TT genotype of AGT" and "body mass index (BMI) < 24" and those who did not--we were able to examine the acquired risk factors for HP during pregnancy in these two groups.
However, in primiparous patients, the frequency was significantly different in elderly pregnancy (63% in severe HP vs. 18% in controls; P < 0.05), in the subgroup with the MM+MT genotypes of the angiotensinogen gene (50% in severe HP vs. 26% in controls; P < 0.05), and in the subgroup with the GA+AA genotypes of the endothelial nitric oxide synthase gene (42% in severe HP vs. 13% in controls; P < 0.05).
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.
Association of a variant of the angiotensinogen gene with pure type of hypertension in pregnancy in the Japanese: implication of a racial difference and significance of an age factor.
In vitro enzymatic studies suggest this mutation would increase production of the vasoactive peptide, angiotensin II in vivo, and therefore explain the etiology of the maternal hypertension.
In the multivariate analysis, FC < or = 10, AC > 10, prepregnancy BMI > or = 24, and homozygosity of the T235 allele genotype of the AGT gene were detected as the potent independent risk factors for HP.
A multivariate analysis with "AC+CC genotype of AT1" and "TT genotype of AGT" revealed that these were independently associated with primiparous severe HP.
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.
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.
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.