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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pregnancy-induced hypertension in women is associated with severe vasoconstriction and reductions in organ blood flow and cardiac output. Recent studies have indicated that nitric oxide (NO) synthesis inhibition during mid to late gestation in pregnant rats results in severe hypertension and proteinuria. The purpose of this study was to determine the systemic hemodynamic and regional blood flow alterations associated with chronic NO synthesis inhibition in the pregnant rat. The study was conducted in four groups of rats: virgin rats (n=6), pregnant rats (n=10), virgin rats treated with L-NAME (n=6), and pregnant rats treated with L-NAME (n=11). Rats were treated with L-NAME in drinking water at a dose of 1 mg/d for a week starting from day 13 of gestation in pregnant rats or an equivalent time for virgins. Mean arterial pressure (MAP), cardiac output, total peripheral resistance (TPR), and regional flows were measured by tracing radiolabeled microspheres in conscious rats. Pregnant rats that were given L-NAME showed significantly higher MAP (137+/-6 versus 96+/-2 mm Hg), higher TPR (5.08+/-0.58 versus 2.90+/-0.44 mm Hg/mL/min/100 g), and lower cardiac output (87.4+/-8.4 versus 113.3+/-11.1 mL/min) than pregnant controls. Chronic NO synthesis inhibition decreased the renal blood flow in pregnant rats at a significantly greater magnitude than in virgin rats. Significant reductions in regional blood flow to the heart, lungs, liver, diaphragm, and skeletal muscles were also observed in pregnant rats treated with L-NAME. The results of this study indicate that NO may play a role in mediating the alterations in systemic hemodynamics and regional blood flow in late pregnant rats.
Hypertension 1998 Jan
PMID:Systemic hemodynamics and regional blood flow during chronic nitric oxide synthesis inhibition in pregnant rats. 945 22

Gestational hypertension and malnutrition are associated with hypertension and ischemic heart disease in the adult human. The impact of the gestational environment on the adult blood pressure in two well-characterized genetically homogeneous rat strains, the hypertensive SS/jr and normotensive SR/jr, was studied by cross-fostering within 6 hours of birth and by embryo transplantation with the recipient dam nursing the transplanted pups. Systolic blood pressure (BP) was measured by tail-cuff plethysmography twice a week after the age of 7 weeks. The lactational environment (cross-fostering) had no effect on blood pressure. Embryo transfer between like strains had no effect on the development of hypertension, nor did the BP of R transferred to S (RetS) differ from that of normal R or RetR. At 7 weeks of age, the BP of SetR was significantly lower than that of S or SetS (P<.01) and was similar to that of RetR and R. With age, the blood pressures of the S, SetS and SetR increased at approximately the same rate but from a significantly different baseline. Salt-sensitivity in the S and resistance in the R were not altered. The protective effect of the R gestational environment on SetR female BP was abrogated during whelping and lactation. Embryo transfer and cross-fostering did not alter the weight of rats older than 7 weeks. Because the BP of the R dams were significantly lower than that of the S dams, these studies do not distinguish between the effects of the R dams' lower blood pressure per se and hormonal influences of the R uterus on the S blood pressure phenotype.
Hypertension 1998 Jan
PMID:Modulation of blood pressure in the Dahl SS/jr rat by embryo transfer. 945 59

Pregnancy-induced hypertension has been suggested to be mediated by several mechanisms, including reduced nitric oxide (NO) synthesis. In this study, the effects of chronic treatment with the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on blood pressure and the underlying changes in vascular reactivity were investigated in virgin and late-pregnancy Sprague-Dawley rats. The systolic blood pressure was 120+/-2, 124+/-5, 116+/-4, and 171+/-5 mm Hg in untreated virgin, virgin treated with L-NAME, untreated pregnant, and pregnant treated with L-NAME rats, respectively. The rats were killed, and the thoracic aorta was cut into strips for measurement of active stress in response to alpha1-adrenergic stimulation with phenylephrine and membrane depolarization by high KCl. In pregnant rats, the maximal active stress to phenylephrine (0.31+/-0.03 x 10(4) N/m2) and the high-KCl-induced active stress (0.55+/-0.09 x 10(4) N/m2) were smaller than those in virgin rats. By contrast, in the L-NAME-treated pregnant rats, the maximal phenylephrine-induced active stress (0.76+/-0.1 x 10(4) N/m2) was greater than that in virgin rats (0.52+/-0.1 x 10(4) N/m2), whereas the high-KCl-induced active stress (1.08+/-0.14 x 10(4) N/m2) was indistinguishable from that in virgin rats (1.03+/-0.14 x 10(4) N/m2). Treatment with L-NAME did not affect the phenylephrine-releasable Ca2+ stores in pregnant rats and had minimal effect on active stress in virgin rats. Thus, reduction of NO synthesis during late pregnancy is associated with a significant increase in blood pressure and vascular responsiveness to alpha-adrenergic stimulation, which can possibly be explained in part by enhanced Ca2+ entry from extracellular space. However, other mechanisms such as increased myofilament force sensitivity to Ca2+ and/or activation of a completely Ca2+-independent mechanism cannot be excluded.
Hypertension 1998 May
PMID:Enhanced vascular reactivity during inhibition of nitric oxide synthesis in pregnant rats. 957 15

Gestational hypertension with or without proteinuria is a multifactorial disease in which the presence of a hypercoagulable state has been suggested. The prothrombin G20210A, the Factor V (FV) Leiden mutations, and the C677T 5-10 methylenetethrahydrofolate reductase (MTHFR) polymorphism were investigated in 140 women with gestational hypertension and in 216 normotensive women from Southern Italy. Nine controls (4.1%) and 16 cases (11.4%; OR: 2.96, 95% CI: 1.27-6.91) carried the prothrombin A20210 allele. FV Leiden mutation was observed in 4 controls (1.8%) and 11 cases (7.9%; OR: 4.53, 95% CI: 1.41-14.53). The TT MTHFR genotype was found in 36 controls (16.6%) and 34 cases (24.4%: OR: 1.61, 95% CI: 0.96-2.74). The impact of potential confounding variables was evaluated using a logistic regression analysis. Nulliparity, Factor V Leiden and prothrombin A20210 carrier status resulted to be independent risk factors of having gestational hypertension with or without proteinuria. Imbalance of haemostasis, through prothrombotic genetic factors, may predispose to the occurrence of gestational hypertension.
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PMID:Prothrombotic genetic risk factors and the occurrence of gestational hypertension with or without proteinuria. 1010 58

We wanted to study if maternal serum mid-trimester total renin, inhibin A, AFP or free beta-hCG levels predict the development of pre-eclampsia. Maternal serum alpha-fetoprotein (AFP) and human chorion gonadotrophin (beta-hCG) were evaluated in the screening programme for Down syndrome in 4356 patients prospectively. Data on pregnancy outcome were available in 1242 women. Pregnancy-induced hypertension (PIH) developed in 69 women, 282 women with uneventful pregnancy outcome were selected for controls. Serum total renin and inhibin A levels were measured retrospectively in the trisomy screening samples of 69 and 30 patients who later developed PIH, and in 282 and 7 patients, respectively, who had an uneventful pregnancy outcome. No significant differences were found in the levels of maternal mid-trimester serum total renin, inhibin A or free beta-hCG levels between PIH and healthy women. The multiples of the median (MoM) of AFP values were significantly higher in the subgroup of patients who later developed severe pre-eclampsia than in patients with mild pre-eclampsia or gestational hypertension and healthy pregnant women. Maternal mid-trimester serum levels of total renin, inhibin A and free beta-hCG are not predictive for development of PIH. High mid-trimester serum AFP values may help in the prediction of severe pre-eclampsia.
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PMID:Prediction of pre-eclampsia with maternal mid-trimester total renin, inhibin A, AFP and free beta-hCG levels. 1021 68

Pregnancy in a woman with Type 1 diabetes poses several clinical challenges. In addition to meticulous glycaemic control, careful attention must be paid to the management of developing and pre-existing diabetic complications which may progress in severity during pregnancy. Pregnancy-induced hypertension is more common in women with diabetes and especially in those with diabetes of long duration. Diabetic renal disease is associated with hypertension which often deteriorates during pregnancy. The management of hypertension is difficult because of limited therapeutic options and the need to consider the implications for the developing fetus as well as the mother. This case report details the clinical management of a young woman with Type 1 diabetes whose pregnancy was complicated by the development of hypertension.
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PMID:The management of hypertension in a diabetic pregnancy. 1036 62

Renal tubular acidosis (RTA) is uncommonly encountered in pregnancy. The risk for these women to develop pregnancy-induced hypertension has not been previously described. The renal defect noted in these women, aggravated by the normal hypervolemia of pregnancy, may predispose to hypertension. Three pregnancies in two women with RTA type 1 developed persistent diastolic hypertension in the third trimester. Mild renal insufficiency was noted in each woman as defined by serum creatinine of 0.9-1.1 and 1.4-1.6 mg/dL, respectively. Vaginal delivery was achieved in each without complications. Blood pressures returned to normal following each pregnancy. Pregnancy-induced hypertension developed in each of three pregnancies in two patients with RTA type 1. The risk for these women to develop pregnancy-induced hypertension may be associated with the higher reported risk in women with underlying renal disease.
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PMID:Pregnancy and renal tubular acidosis. 1045 32

Pregnancy-induced hypertension is associated with increased vascular resistance; however, the cellular mechanisms involved are unclear. We have previously found that the relation between Ca(2+) entry and the developed force in vascular smooth muscle is altered during normal pregnancy and in a rat model of pregnancy-induced hypertension produced by long-term treatment with the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). The purpose of this study was to investigate whether the pregnancy-associated changes in the vascular Ca(2+) entry-force relation reflect changes in the amount and/or activity of Ca(2+)-insensitive protein kinase C (PKC) isoforms. Active stress and the amount and activity of PKC were measured in deendothelialized aortic strips from nonpregnant and pregnant rats untreated or treated with L-NAME and incubated in Ca(2+)-free (2 mmol/L EGTA) Krebs solution. In nonpregnant rats, the PKC activator phorbol 12,13-dibutyrate (PDBu, 10(-6) mol/L) and the alpha-adrenergic agonist phenylephrine (Phe, 10(-5) mol/L) caused significant, maintained increases in active stress and PKC activity that were inhibited by the PKC inhibitors staurosporine and calphostin C. Western blots in aortic strips of nonpregnant rats revealed the Ca(2+)-insensitive delta-PKC and zeta-PKC isoforms. Both PDBu and Phe caused translocation of delta-PKC from the cytosolic to the particulate fraction. Compared with nonpregnant rats, the amount of delta-PKC and zeta-PKC and the PDBu-stimulated and Phe-stimulated stress, PKC activity and translocation of delta-PKC were significantly reduced in late pregnant rats but significantly enhanced in pregnant rats treated with L-NAME. The PDBu-induced and Phe-induced responses in nonpregnant rats treated with L-NAME were not significantly different from nonpregnant rats, whereas the responses in pregnant rats treated with L-NAME+L-arginine were not significantly different from pregnant rats. These results provide evidence that a signaling pathway in vascular smooth muscle possibly involving the Ca(2+)-insensitive delta-PKC and zeta-PKC isoforms is reduced in late pregnancy and enhanced during long-term inhibition of nitric oxide synthesis. The changes in the amount and activity of vascular PKC isoforms may, in part, explain the changes in vascular resistance during normal pregnancy and pregnancy-induced hypertension.
Hypertension 1999 Oct
PMID:Ca(2+)-insensitive vascular protein kinase C during pregnancy and NOS inhibition. 1052 86

We present two cases of Bell's palsy, and another with tinnitus, all in association with pre-eclampsia in the third trimester of pregnancy. We also systematically reviewed the published literature on both Bell's palsy and tinnitus in pregnancy and the puerperium using Medline from January 1966 to October 1998, and searched through the references from review articles and original research publications for further studies. Studies were limited to those published in the English language. We then pooled the rates of occurrence for Bell's palsy according to trimester of pregnancy, and postpartum, as well as the associated prevalence of pre-eclampsia or gestational hypertension. We found that the majority of cases of Bell's palsy arose during the third trimester (pooled event rate 71.1%, 95% confidence interval (CI) 64.1-77.2), while almost none arose in the first trimester. During the postpartum period, the distribution of Bell's palsy was 21.3% (95% CI 15.7-28.1) of all cases, with the majority arising within days of delivery. Gestational hypertension or pre-eclampsia was present in 22.2% of cases (95% CI 12.5-36.4), well above the 5% rate in the general population. Only one paper provided data on tinnitus in pregnancy, with the distribution equal across all three trimesters. When compared to non-pregnant controls, the odds ratio for the development of tinnitus during pregnancy was 2.8 (95% CI 1.0-8.1). In conclusion, Bell's palsy, and perhaps, tinnitus, occur more frequently during the third trimester of pregnancy. Both may be presenting prodromal signs of underlying early pre-eclampsia. The pathophysiologic mechanism relating these two entities to pre-eclampsia is also discussed.
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PMID:Bell's palsy and tinnitus during pregnancy: predictors of pre-eclampsia? Three cases and a detailed review of the literature. 1058 96

The vascular tone depends on periarterial neurogenic nerve stimulus and endothelial substances release. The most evident biochemical cause of the vascular smooth muscle contraction-relaxation process lies in the changing concentration of cytosolic Ca2+. Intracellular free calcium is the major determinant of vascular tone. The depolarization wave opens the slow calcium channels, which permit Ca2+ to enter in small quantities into the interior of the cell triggering the release of much larger quantities of calcium from the sarcoplasmic reticulum. The flux of Ca2+ to and from the cytosol is regulated by three principle mechanisms. The calcium voltage sensitive Ca2+ channel that are opened by the depolarization wave. The potassium channels (CK+) and the Na+/K(+)-ATPase pump. The CK+ opening permits the exit of potassium from the interior of the cell which tends to hyperpolarize the smooth muscle cell membrane and closes the calcium channel avoiding the entry of Ca2+. The activity of the sodium pump also produces membrane hyperpolarization. Thus, the activity of these two mechanisms counter-regulates the voltage dependent calcium channel. The massive release of Ca2+ from intracellular stores of the sarcoplasmic reticulum is done through two classes of channels. One is ryanodine sensitive, the other is the inositol 1,4,5-trisphosphate receptor. The endothelial cell dysfunction is accompanied by a decrease in the production and/or the release of nitric oxide and the increase of contracting factors. That induce a Ca2+ mobilization of extracellular and intracellular stores. Contraction of smooth muscle to hypoxia is mediated by an accumulation of intracellular Ca2+. The relaxant substances of vascular smooth muscle inhibit activation of the phospholipase C and open Ca2+ channels, or produce a stimulus to the exit of the Ca2+ through the plasmatic membrane, with a decrease of intracellular calcium. An endothelial dysfunction with decrease of nitric oxide release exists in different types of hypertension. Pregnancy-induced hypertension is associated with low calcium levels in the diet, improving with the treatment of calcium supplements.
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PMID:[The role of calcium in the regulation of normal vascular tone and in arterial hypertension]. 1061 46


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