L-arginine supplementation lowers blood pressure, protein excretion and plasma lipid profile in experimental salt-induced hypertension in pregnancy: Relevance to preeclampsia

Recent studies have shown that maternal hyperinsulinaemia is a risk factor for the development of hypertension in pregnancy. Experimentally, pregnant rats with chronic exogenously induced hyperinsulinaemia (P-INS rats) have increased blood pressure at the end of gestation. This is associated with a blunted elevation of the excretion of the urinary metabolites of nitrate (UNOx). In the present study, we aimed to evaluate the mechanism(s) of the increase in blood pressure in this model. Four groups were studied: normal pregnant rats (P rats), P-INS rats, P-INS rats treated with l-arginine (2 g/l in the drinking water) (l-ARG rats) and hyperinsulinaemic virgin rats (V-INS rats). Systolic blood pressure (SBP), UNOx excretion (on ingestion of a controlled low-nitrate diet), urine noradrenaline (norepinephrine) and plasma endothelin levels were evaluated. Rats were killed on day 22 of pregnancy. Five P-INS rats were not killed at this time, in order to measure SBP 30 and 60 days after delivery. Fetal number and fetal body weight were evaluated. At the end of pregnancy, a 10±3% increase in SBP was found in P-INS rats, contrasting with a fall of -15±4% in P rats (P < 0.01). In the l-ARG group at the end of pregnancy, SBP values had fallen by -14±2%, to values comparable with those of P rats. The increase in UNOx excretion was 175±38% in P rats, 106±12% in l-ARG rats and 41±8% in P-INS rats (P < 0.01 compared with P and l-ARG groups). No differences were found in the urinary excretion of noradrenaline or in the plasma levels of endothelin-1 between the pregnant groups. Fetal number was similar in all groups, but fetal body weight was lower for P-INS rats compared with P and l-ARG rats. Thus the blood pressure response to l-arginine strongly suggests that a decrease in NO availability may be the main pathogenic mechanism involved in the development of hypertension in this model.

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Managing high blood pressure in pregnancy

Drug and Therapeutics Bulletin ◽

10.1136/dtb.31.14.53 ◽

1993 ◽

Vol 31 (14) ◽

pp. 53-56

Keyword(s):

Blood Pressure ◽

Arterial Blood Pressure ◽

High Blood Pressure ◽

Chronic Hypertension ◽

Pregnancy Induced Hypertension ◽

Hypertension In Pregnancy ◽

Arterial Blood ◽

Induced Hypertension ◽

In Pregnancy

Raised arterial blood pressure is common in pregnancy. Usually it is due solely to the pregnancy and resolves within days or weeks of delivery (pregnancy-induced hypertension – PIH). Occasionally it is chronic hypertension which predates or begins during pregnancy; it persists after delivery. In some women it is a mixture of both, with pregnancy-induced hypertension superimposed on existing chronic hypertension. In this article we discuss the risks to mother and fetus of hypertension in pregnancy and review its prevention and management.

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Abstract P392: Childhood Risk Factors and Adulthood Risk of Pregnancy-Induced Hypertension: The Bogalusa Heart Study

Circulation ◽

10.1161/circ.129.suppl_1.p392 ◽

2014 ◽

Vol 129 (suppl_1) ◽

Author(s):

Shengxu Li ◽

Xu Xiong ◽

Camilo Fernandez ◽

Wei Chen ◽

Sathanur S Srinivasan ◽

...

Keyword(s):

Risk Factors ◽

Blood Pressure ◽

Systolic Blood Pressure ◽

Normal Blood Pressure ◽

Bogalusa Heart Study ◽

Hypertension In Pregnancy ◽

Heart Study ◽

Induced Hypertension ◽

Childhood Risk Factors ◽

In Pregnancy

Background: Hypertension in pregnancy is an important cause of both maternal and fetal morbidity and mortality. Whether hypertension in pregnancy has its risk factor(s) in childhood is not known. The objective of this study was to examine the association between childhood risk factors and hypertension in pregnancy later in life. Methods: A nested case-control analysis was performed based on the longitudinal Bogalusa Heart Study cohort (67% white and 33% black), with an average follow-up period of 26.2 years. Cases were defined as women who had hypertension during pregnancy and had normal blood pressure measurements after the pregnancy (n=82). Controls were defined as women with normal blood pressure without hypertension in pregnancy (n=454). Childhood risk factors included body mass index (BMI), systolic and diastolic blood pressure, high- and low-density lipoprotein cholesterols, and triglycerides. Univariable and multivariable logistic regression were used to estimate the odds ratio (OR) and 95% confidence interval (CI), with childhood risk factors standardized to age- and race-specific z-scores based on the total population of 5419 female subjects. Results: Cases and controls had comparable age in childhood (10.1 vs 9.8 years, P=0.53). Cases vs controls had higher BMI (19.1 vs 17.6 kg/m2, P<0.001) and systolic blood pressure (101.8 vs 99.2 mm Hg, P=0.002) in childhood. In univariable analysis, significant childhood predictors for having hypertension in pregnancy included BMI (OR corresponding to 1 age- and race-specific standard deviation change =1.45, 95% CI: 1.15-1.83) and systolic blood pressure (1.48, 1.15-1.89). BMI and systolic blood pressure remained as significant predictors for having hypertension in pregnancy in multiple regression analysis (1.34, 1.03-1.75 and 1.33, 1.01-1.74, respectively). Conclusions: Childhood BMI and systolic blood pressure are significant predictors for having pregnancy-induced hypertension in adulthood, which underscores the importance of childhood risk factors assessment and early intervention.

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