Hypertension In Late Pregnancy Research Articles

Relationship between serum cystatin C level and pregnancy complications and abnormal glucose tolerance at 6-week postpartum in patients with gestational diabetes mellitus

This study aimed to investigate the relationship between serum cystatin C level and pregnancy complications and abnormal glucose tolerance at 6-week postpartum in patients with gestational diabetes mellitus (GDM). Clinical data of 298 cases of GDM delivered in Taizhou People’s Hospital from January 2017 to June 2018 were retrospectively analyzed. According to the level of cystatin C before delivery, they were divided into normal group (≤ 1.1 mg/L) and elevated group (> 1.1 mg/L). The general situation, complications of pregnancy, and the incidence of abnormal glucose tolerance at 6 weeks after delivery were compared between the two groups. According to concomitant gestational hypertension in late pregnancy, the patients were divided into group A (GDM with hypertensive disorder complicating pregnancy (HDCP)) and group B (GDM without HDCP). The differences of age, parity, body mass index (BMI) and mean arterial pressure (MAP) in the first trimester of pregnancy, levels of cystatin C, creatinine, urinary microalbumin, and glycosylated hemoglobin in 24-week gestation and before delivering were compared between the two groups. There was no significant difference in age and parity between the normal group and the elevated group (p > 0.05). The levels of BMI (25.06 ± 3.46 vs 26.34 ± 3.65 kg/m2), creatinine (38.76 ± 16.52 vs 59.75 ± 17.82 mmol/L), and urinary microalbumin (37.11 ± 49.20 vs 61.25 ± 43.52 mg/L) and the incidence of premature delivery (9.35% vs 17.8%), premature rupture of membranes (11.22% vs 20.94%), and abnormal glucose tolerance at 6-week postpartum (18.69% vs 42.93%) in the normal group of cystatin C were significantly lower than that in the elevated group of cystatin C (p 0.05). The clinical characteristics of group A (GDM with HDCP) and group B (GDM without HDCP) were compared. The results showed that the levels of age, BMI, and mean arterial pressure (MAP) were significantly different (p < 0.001). The results of binary logistic regression analysis showed that the significance value of MAP was 0.005 after controlling age factors, which indicated that MAP was an independent risk factor of GDM with HDCP, and the OR value of MAP was 1.420 (1.109–1.817). The increase of cystatin C in patients with GDM does not increase the risk of HDCP, but it does increase the risks of premature delivery, PROM, and abnormal glucose tolerance at 6-week postpartum. Cystatin C is a biological index that may be valuable in predicting the occurrence of these diseases in GDM patients. The independent risk factor of GDM complicating HDCP is MAP.

Management of acutely decompensated chronic thromboembolic pulmonary hypertension in late pregnancy: a case report

BackgroundPregnancy in patients with pulmonary hypertension is associated with increased risk of maternal and fetal death. Physiological changes during pregnancy, labor and the postpartum period may all lead to acute decompensation of chronic right heart failure with rapid progression to circulatory collapse. As such, guidelines discourage planned pregnancies in women suffering from pulmonary hypertension. There are, however, rare cases of pulmonary hypertension which have previously been undiagnosed and only become apparent during late stage pregnancy. These individuals require close monitoring and multidisciplinary management.Case presentationWe describe the case of a 34-year-old female who presented with acute decompensation of previously undiagnosed pulmonary hypertension during the 30th week of her second pregnancy. Echocardiography and CT scan confirmed severe pulmonary hypertension and right heart failure with no new thromboembolic component. Following stabilization of cardiorespiratory parameters with high FiO2 noninvasive ventilation, intravenous epoprostenol and levosimendan treatment, Cesarean section was performed under epidural anesthesia. Close monitoring was continued in the postoperative period and cardiovascular parameters were managed with ongoing inotropic and escalating vasodilator therapy. The findings were consistent with chronic thromboembolic pulmonary hypertension. Persistent hypoxia was found to be a result of right bronchial obstruction caused by blood clots, which resolved with bronchoscopic intervention. Ongoing postpartum management resulted in improved cardiovascular parameters and oxygenation. Epoprostenol treatment was successfully converted to subcutaneous treprostinil therapy and the patient was discharged home to care for her healthy baby girl. Optimal timing of pulmonary endarterectomy will be chosen based upon functional status and patient preference.ConclusionsThe case described is the first published report of previously undiagnosed pulmonary hypertension presenting with acute right heart failure in late pregnancy successfully managed by pharmacological therapy, noninvasive ventilation and a Cesarean performed under epidural anesthesia. The case illustrates that despite the challenges, acutely discovered right heart failure can be successfully managed with a comprehensive multidisciplinary treatment plan.

SAT-316 MAX-Related Bilateral Pheochromocytoma Associated with Subclinical Adrenal Insufficiency: A Case Report

INTRODUCTION: Loss-of-function mutation in the MYC-associated factor X (MAX) gene causes hereditary pheochromocytoma (PCC) that are frequently bilateral or multifocal1. Adrenal insufficiency (AI) associated with unresected bilateral PCC has not been previously described. We hereby present a case of subclinical AI in a patient with bilateral PCC. CLINICAL CASE: An otherwise healthy 30-year-old woman was found to have a pathogenic MAX gene mutation (c.228delG) after undergoing genetic testing for a significant family history of PCC in 3 relatives. She participated in high-intensity interval training 5 times per week and denied episodes of palpitations, flushing, diaphoresis, or dizziness, but endorsed frequent pulsatile tinnitus and morning headaches. She had a history of hypertension in late pregnancy which had been presumed gestational. Exam was notable only for manual BP 152/110 mmHg, HR 110 bpm, and a faint resting tremor. Lab work was consistent with PCC: plasma norepinephrine 12417 pg/mL (ref <874) and normetanephrine 26 nmol/L (ref <0.9); urine norepinephrine 3378 mcg/24h (ref <135) and normetanephrine 16620 mcg/24h (ref <500). AM cortisol was 10.9 mcg/dL (ref 5-20) with a high normal ACTH of 46 pg/mL (ref 0-46) and low DHEA-S of 23 mcg/dL (ref 75-530). She had no prior history of glucocorticoid exposure, and thyroid studies were normal. CT imaging revealed bilateral contrast-enhancing heterogeneous adrenal masses (R: 3.5 x 2.2 cm; L: 4.6 x 4.5 cm). She was treated with alpha- then beta-adrenergic blockade and subsequently underwent surgical removal of both adrenal tumors with sparing of the superior adrenal cortices bilaterally. Plasma and urine catecholamines and metanephrines normalized a week post-operatively, and she began to report fatigue and dizziness. Two weeks post-operatively, midday plasma levels of cortisol, DHEA-S, and ACTH were 6.3 mcg/dL, <15 mcg/dL, and 118 pg/mL, respectively. Standard-dose 250mcg ACTH stimulation test confirmed AI with peak cortisol of 15.1 mcg/dL. Replacement hydrocortisone was initiated with prompt resolution of symptoms. CONCLUSIONS: Individuals with a pathogenic MAX mutation require prompt screening for PCC as symptoms may be subtle despite significant biochemical abnormalities. Large PCCs may also impact hormone synthesis by the adjacent adrenal cortex. Even prior to surgery, this patient had subclinical AI as evidenced by a high-normal plasma ACTH and clearly low DHEA-S. The latter is the earliest adrenal steroid to decline in patients with primary or central AI2. It is unclear whether her worsening adrenal function after surgery was a surgical complication or due to dramatic decline in circulating catecholamines. Regardless, loss of adrenal androgen production warrants close follow-up for development of AI. REFERENCES: (1) Burnichon N et al. Clin Cancer Res 2012;18:2828 (2) Sayyed Kassem L et al. JCEM 2012;97:3655

Angiotensin II accelerates mammary gland development independently of high blood pressure in pregnancy-associated hypertensive mice.

Angiotensin II (AngII) is a vasopressor hormone that has critical roles in maintenance of normal blood pressure and pathogenesis of cardiovascular diseases. We previously generated pregnancy-associated hypertensive (PAH) mice by mating female human angiotensinogen transgenic mice with male human renin transgenic mice. PAH mice exhibit hypertension in late pregnancy by overproducing AngII. A recent study demonstrated that angiotensin II type I (AT1) receptor is expressed in mammary epithelial cells and its signaling is critical for mammary gland involution after weaning. However, the role of AngII-AT1 receptor signaling in the development of mammary gland during pregnancy remains unclear. In this study, to investigate the role of AngII-AT1 receptor signaling in mammary gland development during pregnancy, we analyzed the mammary gland of PAH mice. Histological and gene expression analyses revealed that lobuloalveolar development was accelerated with increased milk protein production and lipid accumulation in the mammary gland of PAH mice. Furthermore, AT1 receptor blocker treatment suppressed acceleration of mammary gland development in PAH mice, while the treatment of hydralazine, another antihypertensive drug, did not. These data suggest that AngII-AT1 receptor-induced signaling accelerates mammary gland development during pregnancy through hypertension-independent mechanism.

Short-term suppression of the renin-angiotensin system in mice associated with hypertension during pregnancy

Pregnancy-induced hypertension or pre-eclampsia is a major disorder that may result in serious complications for the mother and fetus. It is characterized from maternal hypertension in late pregnancy and peripheral tissue damage, including kidney, heart and placenta, and the fetus suffers from intrauterine growth retardation (IUGR) and high perinatal mortality. Recently, it has been postulated that angiotensin II (Ang II), a potent vasoconstrictor in the renin-angiotensin system (RAS), plays a pivotal role in the pathogenesis of pre-eclampsia; however, the beneficial effect of the suppression of RAS has not yet been fully elucidated. Previously, we generated a transgenic mouse model that developed pregnancy-associated hypertension (PAH) by the overproduction of Ang II in maternal circulation during late pregnancy. In addition, mice with PAH exhibited maternal and fetal abnormalities, such as proteinuria, cardiac hypertrophy, placental morphological changes and IUGR. In this study, in order to attenuate the activity of redundant RAS during the advanced stages of PAH, we administered olmesartan (Olm), an angiotensin receptor blocker, and captopril (Cp), an angiotensin converting enzyme inhibitor, from E17 to E19 days of gestation, and evaluated its effect on cardiac and placental abnormalities and fetal growth. Olm and Cp administration significantly lowered the blood pressure of mice with PAH, and placental histological change and severe IUGR were markedly ameliorated in both groups. On the contrary, Olm or Cp treatment had little effect on cardiac remodeling during the advanced stages of PAH. These findings highlight a variety of therapeutic actions of RAS repression on the progressive pathology of PAH in mice.

Vitamin D and hypertension in pregnancy

Vitamin D Deficiency is common, particularly in northern latitudes. We examined the association between vitamin D status and hypertension in late pregnancy. A case-control study was conducted during two time periods: September-October, 2008, and January-March, 2009, in women near term. A case was defined as having two or more documented blood pressure readings above 140/90 (either/or) at any time during pregnancy (n=78). Controls had at least two blood pressure readings, with none above 140/90 during pregnancy (n=109). Serum 25-hydroxyvitamin D (25(OH)D) was measured in all participants. In the summer, 13% of controls and 29% of the cases had 25(OH) D levels < 50 nmol/L. During the winter, these numbers rose to 44% and 49% respectively. Both cases and controls were more likely to be vitamin D deficient in the winter (p=0.002). There was a negative correlation between BMI and 25(OH)D (r=-0.202, p=0.002). In univariate analysis, cases had lower 25(OH)D (p=0.046), but also higher body mass index, so that in multivariate analysis 25(OH)D status was no longer significant. There was no difference in mean oral daily vitamin D intake (dietary intake and supplements, 746 and 785 IU respectively). Controls gained less weight in pregnancy. There was a negative correlation between the highest blood pressure measured in pregnancy and 25(OH)D levels (r= -0.118; p=0.012). There is a high prevalence of vitamin D deficiency in pregnant women recruited in Saskatoon, Saskatchewan. Women with low circulating vitamin D concentrations are more likely to have hypertension.

Quantification of proteinuria in mild preeclampsia with random albumin creatinine ratio

Objective: To investigate the whether spot urinealbumin/creatinine ratio (ACR) compared to the 24hurinary protein (gold standard) to detect significantproteinuria in patients with preeclampsia. Study design:80 pregnant patients diagnosed to have hypertension inlate pregnancy were instructed to collect urine during a24-hour period. Albumin creatinine ratio was evaluatedin a random urinary specimen and morning samples forquantization of proteinuria. Out of these, 78 patientsfulfilled the inclusion criteria. The predictive value of therandom urinary ACR for the diagnosis of significantproteinuria was estimated by using various cutoff valuesof urinary ACR in comparison to 24-h urine collection asthe gold standard. Results: 70 (89%) patients had preeclampsia. The meanmorning systolic blood pressure on the day of the urinecollections was 150 mmHg and mean diastolic bloodpressure 114 mmHg. The mean total protein was1961.46+1683.02 mg/24h, and the urinary ACR inrandom samples was 781.31+1041 mg/g creatinine,while in the morning sample urinary ACR was886.43+1180.9 mg/g creatinine. There was a statisticallysignificant positive correlation between in 24-hours urineproteins and ACR in both daytime and morning urinesamples. The best cutoff point for ACR in randomsample was 262.5 mg /g creatinine as with a sensitivityof 85.5% and a specificity of 81.8%, the positivepredictive value was 96.7% and negative predictive valuewas 47.4%. While the best cutoff point for ACR inmorning sample was 240 mg /g creatinine with asensitivity of 94.2% and a specificity of 63.6%, thepositive predictive value was 94.2% and negativepredictive value was 63.6%. Conclusion: Albumin/creatinine ratio is not an ideal diagnostic test to replace 24-hour urine collection for the diagnosis of preeclampsia. However, it can be used as a screening test with sensitivity 94% when the cut point of albumin/creatinine ratio of the morning urine sample is set below 240 mg/g creatinine.

New-Onset Hypertension in Late Pregnancy and Fetal Growth: Different Associations Between Singletons and Twins

Objective: To compare the effects of new-onset hypertension (NOH) in late pregnancy on fetal growth in singletons and twins. Methods: A retrospective cohort study was conducted to evaluate the effect of NOH on fetal growth in 17, 720, 900 singletons and 463, 104 twins born in the United States between 1995 and 2000. Results: NOH was associated with lower mean birth weight in both preterm and term singletons. Increased risk of low birth weight and decreased risk of high birth weight was associated with NOH in preterm and term singletons. NOH was associated with increased risk for small-for-gestational-age (SGA) births and decreased risk for large-for-gestational-age (LGA) births in preterm singletons, whereas it was associated with increased risk of both SGA and LGA births in term singletons. NOH was associated with higher mean birth weight in early preterm twins, and lower mean birth weight in term twins. Decreased risk for low birth weight was found in the NOH group among early preterm twins, and increased risk for low birth weight in term twins. NOH was associated with increased risk of SGA births and decreased risk for large-for-gestational-age (LGA) births in early preterm twins, while increased risk of SGA births in term twins. Conclusion: NOH is associated with slower fetal growth in singletons delivered at different gestational ages, but the effect varies in twins depending on gestational age at delivery with faster growth in early preterm twins.

Maternal Age, Paternal Age and New-Onset Hypertension in Late Pregnancy

Objective: To examine the association between maternal age, paternal age, and new-onset hypertension in late pregnancy. Methods: We carried out a retrospective cohort study of 9,302,675 pregnant women with live births in the United States between 1995 and 1998. Maternal and paternal ages were analyzed together using “couple age” in multivariate logistic regression models to reduce colinearity between maternal age and paternal age. The effect of paternal age was also analyzed with stratification of maternal age. Results: Compared with couples with both a maternal and paternal age of 20 to 34 years, an older maternal age (above 35 years) was associated with an increased risk for new-onset hypertension, except for couples with a very young father (below 20 years). Younger maternal age (below 20 years) was associated with a decreased risk for new-onset hypertension, except for couples with a very old father (above 45 years). There was no significant association between paternal age and new-onset hypertension with stratification of maternal age. Conclusion: Increased risk for new-onset hypertension in late pregnancy is significantly associated with advancing maternal age, whereas there is no association between paternal age and new-onset hypertension in late pregnancy.

New-Onset Hypertension in Late Pregnancy is Associated with Lower Fetal and Infant Mortality in Preterm Twins

Objective: To assess the association between new-onset hypertension in late pregnancy (NOH) and fetal and infant mortality in early preterm, late preterm, and full-term twins. Methods: We conducted a retrospective cohort study in 275, 316 twins in 1995–1997 based on multiple birth registration dataset of USA. Generalized estimating equations (GEEs) was used to evaluate the odds ratios (OR) of fetal and infant death (at individual level) associated with NOH, with adjustment of potential confounders at both twin set level and individual level. Results: The risks for early neonatal death (OR = 0.52, 95% CI: 0.36, 0.76) and late neonatal death (OR = 0.57, 95% CI: 0.37, 0.87) were decreased in early preterm twins born to mothers with NOH compared with early preterm twins born to mothers with normal blood pressure. The decreased risks for fetal death (OR = 0.40, 95% CI: 0.30, 0.53; OR = 0.46, 95% CI: 0.53, 0.65) and infant death (OR = 0.35, 95% CI: 0.28, 0.44; OR = 0.68, 95% CI: 0.51, 0.91) were associated with NOH in both early and late preterm twins, whereas no association between NOH and fetal/infant mortality were observed in full-term twins. Conclusion: NOH is associated with lower risk of fetal death and infant death in preterm twins.

An essential role for angiotensin II type 1a receptor in pregnancy-associated hypertension with intrauterine growth retardation.

Little is known about an in vivo significance of angiotensin II Type-1 receptor (AT1) for pregnancy-associated diseases, including hypertension and intrauterine growth retardation (IUGR). We previously demonstrated that female mice carrying the human angiotensinogen gene (hAG+/+), when mated with human renin transgenic (hRN+/+) male mice, displayed hypertension in late pregnancy due to secretion of human renin from the fetal side into the maternal circulation. In the present study, to investigate a role for AT1 in pregnancy-associated hypertension, we generated a new strain of hAG+/+/mAT1a-/- mice by genetically deleting the AT1a gene from hAG+/+ mice. When mated with hRN+/+ male mice, excessive increases in human renin, angiotensin, and plasma renin activity were detected in the plasma of pregnant hAG+/+/mAT1a-/- mice as found in that of pregnant hAG+/+ mice. Surprisingly, however, blood pressure of hAG+/+/mAT1a-/- mice was not elevated in late pregnancy despite the presence of AT1b, a subtype of AT1. The maternal and fetal defects, such as cardiac and placental abnormalities, and IUGR observed in pregnant hypertensive hAG+/+ mice were not recognized in pregnant hAG+/+/mAT1a-/- mice. The limited term administration of AT1 antagonists to hypertensive hAG+/+ mice in late pregnancy dramatically improved hypertension and IUGR, showing the clinical importance of AT1a.

Renal function following pregnancy in renal transplant recipients

We set out to analyse the effect of pregnancy and hypertension in renal transplant recipients and review serum creatinine levels as a marker of graft function, before, during and after pregnancy. The study was conducted at a major tertiary referral centre in London. This was a retrospective analysis of renal transplant patients who had achieved a successful pregnancy. During the period 1967-1998, there have been 272 women of childbearing age with successful renal transplants functioning for over 1 year. Within this population there have been 66 pregnancies in 41 patients resulting in 53 births. Among the pregnancies that progressed beyond 24 weeks, preterm delivery occurred in 32 (60·4%). The mean gestation was 35·7 (range 30-41), mean birth weight was 2365 grams (range 908-3430 grams) with 47%of infants weighing <2500 grams. There were vaginal deliveries in 14 (26%), the rest delivered by caesarean section. Patients that developed hypertension in late pregnancy tended to have higher pre-pregnancy creatinine levels and a deterioration of graft function postpartum. Serum creatinine levels greater than 130 w mol/l before pregnancy predict deteriorating renal function postpartum. Kaplan-Meier life survival analysis showed that the risk of subsequent graft loss is associated with increased serum creatinine levels (130-180 w mol/l) before pregnancy. Pregnancy figures in our unit are favourable compared to those reported in the literature. Poor pre-pregnancy renal function (creatinine 130-180 w mol/l) and previous hypertension is associated with a significant risk of graft failure. Creatinine levels currently deemed as being acceptable during the pregnancy of renal transplant recipients may need to be reappraised.

A randomized comparison of early with conservative use of antihypertensive drugs in the management of pregnancy-induced hypertension

Summary. Two treatment strategies were compared in 155 women with pregnancy-induced hypertension who were also given comprehensive non-pharmacological care. The mean gestation at entry was 28 weeks. As long as the diastolic blood pressure (DBP) remained below 106 mmHg, oxprenolol, or oxprenolol plus dihydralazine, were given to the early treatment group, and matching placebos to the control group. Open antihypertensive treatment was provided for patients whose DBP rose above 105 mmHg. Proteinuria occurred in seven women in each group. In the early treatment group, 13 of the 78 women were delivered by caesarean section; the corresponding numbers in the control group were 27 of 76 (17 vs 36%, 95% confidence interval (CI) of difference: 5-33%); the sections included seven and 16 in the early treatment and control groups, respectively, for severe hypertension and/or fetal distress. There were five perinatal deaths, two in the early treatment group and three in the control group. Early treatment did not influence gestational age at birth or birthweight. Respiratory distress syndrome occurred in four infants in the early treated group and in 10 in the control group; 14 infants in the former group and 26 in the latter were in hospital for more than 10 days (18 vs 35%; 95% CI of difference 4.32%). These results indicate that early antihypertensive treatment with oxprenolol is safe for the fetus and newborn in pregnancy-induced hypertension, but has no advantage over non-pharmacological care in terms of fetal growth. However, it may prevent acute hypertension in late pregnancy and associated fetal distress, and thus reduce the number of caesarean sections.

A randomized comparison of early with conservative use of antihypertensive drugs in the management of pregnancy‐induced hypertension

Two treatment strategies were compared in 155 women with pregnancy-induced hypertension who were also given comprehensive non-pharmacological care. The mean gestation at entry was 28 weeks. As long as the diastolic blood pressure (DBP) remained below 106 mmHg, oxprenolol, or oxprenolol plus dihydralazine, were given to the early treatment group, and matching placebos to the control group. Open antihypertensive treatment was provided for patients whose DBP rose above 105 mmHg. Proteinuria occurred in seven women in each group. In the early treatment group, 13 of the 78 women were delivered by caesarean section; the corresponding numbers in the control group were 27 of 76 (17 vs 36%, 95% confidence interval (CI) of difference: 5-33%); the sections included seven and 16 in the early treatment and control groups, respectively, for severe hypertension and/or fetal distress. There were five perinatal deaths, two in the early treatment group and three in the control group. Early treatment did not influence gestational age at birth or birthweight. Respiratory distress syndrome occurred in four infants in the early treated group and in 10 in the control group; 14 infants in the former group and 26 in the latter were in hospital for more than 10 days (18 vs 35%; 95% CI of difference 4-32%). These results indicate that early antihypertensive treatment with oxprenolol is safe for the fetus and newborn in pregnancy-induced hypertension, but has no advantage over non-pharmacological care in terms of fetal growth. However, it may prevent acute hypertension in late pregnancy and associated fetal distress, and thus reduce the number of caesarean sections.

Acute effects of dihydralazine mesylate, furosemide, and metoprolol on maternal hemodynamics in pregnancy-induced hypertension

The intervillous blood flow and other maternal hemodynamic parameters were assessed in 40 mothers with pregnancy-induced hypertension in late pregnancy before and after hypotensive treatment. Furosemide caused a significant decrease in the intervillous blood flow, whereas the effects of dihydralazine and metoprolol were both negative and positive, that is, more individual and diverse. These changes in the intervillous blood flow did not have any correlation with the changes in other maternal hemodynamic parameters. The importance of placental hemodynamic studies in the evaluation of hypotensive drugs is stressed.

The platelet count and mean platelet volume.

The Coulter Model S-Plus Counter provides a measure of the platelet count and the mean platelet volume (MPV). An analysis of 5000 unselected blood specimens showed an inverse relationship between the number of circulating platelets and their MPV. In nearly 95% of normal adults the platelet count varied from 150 to 450 X 10(9)/l and the MPV from 7.0 to 10.5 fl. Thrombocytosis was found in iron deficiency anaemia, after trauma and acute blood loss and in rhematoid arthritis. Although there is a normal platelet distribution in pregnancy, patients with pre-eclampsia and uncomplicated hypertension in late pregnancy tended to have lower platelet counts and larger platelets than controls. A variable platelet pattern was found in infection, renal failure and treated malignant disease.

Plasma noradrenaline in normal pregnancy and in hypertension of late pregnancy.

Plasma noradrenaline was measured by radioenzymatic assay on 90 occasions in 72 women throughout normal pregnancy. Plasma noradrenaline levels declined as pregnancy advanced. A total of 21 patients who developed hypertension in late pregnancy were found to have plasma noradrenaline levels significantly lower than controls at the same stage of pregnancy. It is concluded that plasma noradrenaline is reduced in hypertension of late pregnancy. This indicates a compensatory reduction in sympathetic nervous system activity.

Modern Trends in Management of Non-Albuminuric Hypertension in Late Pregnancy

Modern Trends in Management of Non-Albuminuric Hypertension in Late Pregnancy

Modern Trends in Management of Non-Albuminuric Hypertension in Late Pregnancy

Modern Trends in Management of Non-Albuminuric Hypertension in Late Pregnancy

Modern trends in management of non-albuminuric hypertension in late pregnancy.

Modern trends in management of non-albuminuric hypertension in late pregnancy.