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

Recent evidence indicates that transforming growth factor-beta 1 (TGF-beta 1) plays an important role in renal fibrosis via stimulation of extracellular matrix synthesis. The present study was undertaken to investigate the role of angiotensin II type I receptor (AT1 receptor) in hypertension-induced renal injury. Twenty-two-week-old stroke-prone spontaneously hypertensive rats (SHRSP), which had established hypertension and moderate renal damage, were orally given TCV-116, a selective non-peptide AT1 receptor antagonist (0.1, 1 or 10 mg/kg/day), enalapril (10 mg/kg/day) or vehicle once a day for 10 weeks. At the end point of the treatment, we examined renal function, the gene expressions of TGF-beta 1 and extracellular matrix components in the interstitium [collagen types I (COI) and III (COIII), fibronectin (FN)] and the basement membrane (COIV and laminin), and renal microscopic morphology in rats aged 32 weeks. In vehicle-treated 32 week-old SHRSP with renal dysfunction and nephrosclerosis, renal mRNA levels for TGF-beta 1, COI, COIII, FN, COIV were all several-fold higher than in WKY. Thus, renal TGF-beta 1 gene expression was enhanced in SHRSP, which may contribute to the increased renal expressions of COI, COIII, FN, COIV in SHRSP. Treatment with TCV-116 (0.1 mg/kg/day) in SHRSP, in spite of no reduction of blood pressure, decreased renal mRNA levels for TGF-beta 1, COI, COIII, FN, COIV, being accompanied by the significant decrease in urinary protein and albumin excretion, blood urea nitrogen and plasma creatinine. Treatment with TCV-116 (10 mg/kg/day) in SHRSP decreased mRNAs for TGF-beta 1, COI, COIII, FN and COIV to almost the same levels as WKY, being associated with normalization of urinary protein and albumin excretion and the prevention of nephrosclerosis, as judged by microscopic histological observations. On the other hand, the effects of enalapril (10 mg/kg/day) on the above mentioned mRNA levels, renal function and renal morphology were weaker than those of TCV-116 (10 mg/kg/day) and were as much as TCV-116 (1 mg/kg/day). These results suggest that independently of hypotensive action, AT1 receptor antagonist has a potent renal protective effect by inhibiting the gene expression of renal TGF-beta 1 and extracellular matrix components.
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PMID:Contribution of renal angiotensin II type I receptor to gene expressions in hypertension-induced renal injury. 785 93

Cord blood samples were estimated for serum fibronectin (Fn) by immunoelectrophoresis (IE) and enzyme linked immuno sorbent assay (ELISA) in 250 newborn healthy and sick infants classified into 6 categories: i.e., term appropriate for date (TAFD), preterm appropriate for date (PTAFD), term small for date (TSFD), preterm small for date (PTSFD), birth asphyxia (BA) and septicemia (SEP). TAFD infants were assayed for plasma Fn in addition. Comparison of Fn levels in the different groups by the Wilcoxan rank sum test indicated no significant difference between term and preterm infants, between PTAFD and PTSFD, TAFD and TSFD and in infants with and without birth asphyxia. Babies with septicemia had a significantly (P < 0.01) lower Fn level (29.97 +/- 29.03 mg/l) than those with no septicemia (42.77 +/- 30.20 mg/l). TAFD infants had Fn levels (serum 41.44 +/- 31.08 mg/l, plasma 85.20 +/- 33.38 mg/l) that are less than half the levels reported in the Western literature for newborn term infants. A possible cause could be the associated medical problems in mothers as 41 per cent of mothers of TAFD infants had conditions such as pregnancy induced hypertension, gestational diabetes, rheumatic heart disease, infection etc.
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PMID:Fibronectin levels in Indian neonates in health & disease. 792 72

Effects of hypertension and aging on aortic fibronectin expression were investigated in male Dahl salt-sensitive (Dahl-S) and salt-resistant (Dahl-R) rats fed either a low- or high-salt diet from 5 to 37 wk of age. In comparison to low-salt controls, the steady-state mRNA levels for aortic fibronectin in salt-loaded Dahl-S rats were dramatically increased at 37 wk of age, corresponding to a severe stage of hypertension with high mortality, whereas at earlier ages representing early to established phases of hypertension, no significant changes were observed. Salt loading affected neither blood pressure nor aortic fibronectin expression in Dahl-R rats. Aging without coexisting hypertension did not cause significant changes in aortic fibronectin mRNA levels all through the study period in either strain of rats. These results suggest that aortic fibronectin may be strongly regulated by factors associated with severe hypertensive organ damages caused by long-standing hypertension in salt-loaded Dahl-S rats. Also suggested was that aortic fibronectin may not play a major role in the pathogenesis of early aortic changes occurring in response to hypertension or as a process of aging.
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PMID:Effects of hypertension and aging on fibronectin expression in aorta of Dahl salt-sensitive rats. 794 97

The diagnosis of preeclampsia, with all of its consequences, is at times difficult to establish, especially when the patient has underlying chronic hypertension and is not known from prior prenatal care visits. Many screening tests have been proposed. These should be sensitive, relatively specific, easy to perform, of low cost, and have a reasonable interval from prediction to disease onset. Laboratory assays would obviously be useful. We evaluated hemostasis tests for the diagnosis of preeclampsia, and compared fibronectin, antithrombin III and alpha 2-antiplasmin in 48 preeclamptics and 86 control nulliparas. Receive operator characteristic (ROC) curve analysis suggested that fibronectin is the most effective of these tests. A similar analysis comparing the results of previous studies using serum iron, angiotensin infusion, urinary calcium/creatinine ratio, the rollover test and uric acid suggested a possible role for fibronectin in the diagnosis of preeclampsia. While not ideal, there seems to be, at present, no other, easy to perform laboratory test that outperforms fibronectin in predicting preeclampsia.
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PMID:Hemostasis and diagnosis of preeclampsia. 797 90

In this study we evaluated fibronectin as a marker of endothelial cell injury and antithrombin III as a marker of chronic activation of intravascular coagulation. The aim of the study was to establish to normal trends of plasma antithrombin III and fibronectin in general obstetric population and to determine the value of both in predicting, distinguishing and understanding the pathophysiology of pregnancy induced hypertension. The all cases consisted of 173 pregnant, 19 of them were chronic hypertensive, 45 were pregnancy induced hypertensive and 119 were normotensive at blood sampling. Out of 119 normotensive cases, 109 cases had no adverse outcome during their pregnancy. These cases were used as a control group and for the normal trends of antithrombin III and fibronectin in general obstetric population. Ten out of 119 cases who developed preeclampsia during follow up, 19 cases with chronic hypertension and 45 cases with pregnancy induced hypertension consisted of the study group. In the cases who developed preeclampsia during follow up, the value of plasma fibronectin level (above 95% confidence limit for that gestational week) to predict preeclampsia had 90% sensitivity and 94.4% specificity. In distinguishing hypertensive disorders of pregnancy (chronic hypertension or pregnancy induced hypertension) fibronectin had 71.1% sensitivity and 100% specificity. Plasma antithrombin III level (of antigenicity) measured by immunodiffusion method had no value in predicting and distinguishing pregnancy induced hypertension.
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PMID:The value of antithrombin-III and fibronectin in hypertensive disorders of pregnancy. 803 92

To investigate the role of angiotensin II (Ang II) in hypertension-induced tissue injury, we gave TCV-116 (1 mg/kg per day PO), a nonpeptide Ang II type I receptor antagonist, or enalapril (10 mg/kg per day PO) to deoxycorticosterone acetate (DOCA)-salt hypertensive rats for 3 weeks and examined the effects on tissue mRNA levels for transforming growth factor-beta 1 (TGF-beta 1) and extracellular matrix components. Tissue mRNA levels were measured by Northern blot analysis. Renal mRNA levels for TGF-beta 1; types I, III, and IV collagen; and fibronectin in DOCA-salt hypertensive rats were increased by severalfold (P < .01) compared with sham-operated rats. In the aorta of DOCA-salt hypertensive rats, TGF-beta 1 and fibronectin mRNA levels were increased, but types I, III, and IV collagen mRNAs did not increase. In the heart, increased mRNA was found only for fibronectin. Thus, these gene expressions are regulated in a tissue-specific manner. TCV-116 or enalapril did not lower blood pressure in DOCA-salt hypertensive rats. However, the increase in renal mRNAs for TGF-beta 1 and extracellular matrix components in DOCA-salt hypertensive rats was significantly inhibited by treatment with TCV-116 or enalapril, which was associated with a significant decrease in urinary protein and albumin excretions and histological improvement of renal lesions. In contrast, in the aorta and heart these gene expressions were not affected by TCV-116 or enalapril. Thus, local Ang II may contribute to renal injury of DOCA-salt hypertension by stimulating the gene expression of TGF-beta 1 and extracellular matrix components.
Hypertension 1994 Aug
PMID:Role of angiotensin II in renal injury of deoxycorticosterone acetate-salt hypertensive rats. 803 44

1. Fibronectin does not correlate with the grade of proteinuria. 2. Fibronectin does not correlate with birth weight. 3. Fibronectin level is not elevated in pregnancy-induced hypertension and preeclampsia. 4. Fibronectin level is elevated in cases of preeclampsia, combined with chronic placental insufficiency respectively intrauterine growth retardation. 5. There is a statistic significant difference between pregnancy-induced hypertension/preeclampsia with or with out placental insufficiency. 6. Extremely problematic pregnancies ended in all pregnancies with values of fibronectin above 0.4 g/l in caesarean section without knowledge of the elevated fibronectin level at the time of operation. 7. In the group of pregnancy-induced hypertension the fibronectin level is elevated in relation to control group. This increase is particularly evident, if a placental insufficiency is concontinant with preeclampsia.
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PMID:[Critical evaluation of fibronectin in pregnancy-induced hypertension/pre-eclampsia and placental insufficiency]. 804 91

We have measured plasmatic fibronectin in 23 normotensive pregnant women during pregnancy (overall 161 values). On the average 6 samples from every woman have been taken. Plasmatic fibronectin rose continuously from 313 +/- 76 mg/l in the first trimester to 416 +/- 194 mg/l in the third trimester. Normal pregnant women (n = 173, 358 +/- 140 mg/l) were compared with pregnant patients with preeclampsia (n = 37), woman with chronic hypertension in pregnancy (n = 25) and normotensive pregnant patients with intrauterine growth retardation (IUGR, n = 5). In the group with chronic hypertension (466 +/- 119 mg/l) there was no significant difference to the normal group, but we found a significant (p < 0.01) different value of fibronectin (748 +/- 195 mg/l) in the group of patients with preeclampsia. A tendency to higher fibronectin values was also noticed in the group with IUGR (739 +/- 212 mg/l). Because of the low number of patients this difference was not statistically significant. We conclude, that plasmatic fibronectin is an important, but not absolutely specific screening parameter for estimation of the endothelial injury in hypertensive disorders of pregnancy. We believe, that fibronectin is one the best parameters to forecast a preeclampsia.
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PMID:[The clinical value of plasma fibronectin in pregnancy]. 804 92

Gestational proteinuric hypertension (GPH), a major cause of maternal death, may be characterised by hypertension and proteinuria alone or may progress to disturbed coagulation and multiorgan failure. Since the condition can only be reversed by termination of pregnancy, there is a need for reliable indicators of severity. We found circulating levels of tissue plasminogen activator (tPA) (27.98 +/- 2.12 v. 7.17 +/- 0.81 ng/ml, mean +/- SEM), fibrin(ogen) degradation products (FDP) (7.55 +/- 1.99 v. 1.92 +/- 0.47 micrograms/ml) and fibronectin (221 +/- 15.2 v. 120 +/- 15.2 micrograms/ml) to be significantly increased in 21 patients with severe GPH when compared with 21 normotensive, age- and gestational age-matched pregnant controls. More importantly, patients who developed severe GPH showed a progressive increase in tPA and FDP levels with time. This was in contrast to patients who had hypertension and proteinuria alone, in whom tPA and FDP concentrations did not increase. Parallel measurements did not reveal a fall in platelet count or an increase in urinary protein excretion in patients who subsequently progressed to severe disease. Our findings may be of assistance to clinicians faced with the need to prolong pregnancy in patients with GPH in order to ensure fetal viability.
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PMID:Serial measurements of circulating tissue plasminogen activator and fibrin(ogen) degradation products predict outcome in gestational proteinuric hypertension. 811 15

Smooth muscle cells (SMCs) of rabbit aorta undergo marked changes in myosin isoform content during development. Analysis of nonmuscle myosin composition at the protein level has permitted the identification of three phases in the SMC differentiation process: fetal, postnatal, and adult. Using monoclonal antibodies specific for smooth muscle and nonmuscle myosins and extra domain A of fibronectin as well as cDNA probes for platelet-derived growth factors (PDGF) and various procollagens, we have evaluated the differentiation pattern of aortic SMCs in two-kidney, one-clip hypertensive rabbits. Morphometric and bromo-deoxyuridine studies indicate that hypertrophy of aortic media along with intimal thickening occurring in hypertensive animals is due to SMC hyperplasia. Western blotting experiments performed on aortic specimens from hypertensive animals with antimyosin antibodies revealed the appearance of a myosin isoform pattern of the "immature" type. Immunofluorescence tests showed that these cells are localized in the thickened intima or distributed in the underlying media (sparsely or in groups). Similarly, the fibronectin variant showing the extra domain A, peculiar to "phenotypically modulated" SMCs, appeared in intimal thickening, and its expression followed the time course of nonmuscle myosin expression. Counting of postnatal-type SMCs in the aortic media revealed that this cell population increases markedly with hypertension (2- up to 15-fold at 4 months) and then declines to near control level in 8-month hypertensive rabbits. Diminution of postnatal-type SMCs at later stages of hypertension was temporally correlated with the slowing down of aortic wall hypertrophy. Average levels of mRNAs, as determined by densitometric analysis in aortas from 1- and 2.5-month hypertensive rabbits, showed an increased expression for PDGF beta receptor (up to twofold), procollagen type I (alpha 1, threefold), procollagen type III (alpha 1, twofold), and fibronectin (up to threefold) compared with controls. Conversely, the steady-state levels of mRNAs for PDGF (A and B chain), PDGF alpha receptor, TGF-beta 1, and procollagen type IV (alpha 1) did not increase significantly. These results provide evidence that in adult renovascular hypertensive rabbits, the hyperplastic growth of aortic SMCs is accompanied by the expansion of an "immature" cell phenotype characteristic of the early stages of development.
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PMID:Hyperplastic growth of aortic smooth muscle cells in renovascular hypertensive rabbits is characterized by the expansion of an immature cell phenotype. 815 26


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