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

Several methods used in the prediction of hypertensive disorders of pregnancy (HDP) were evaluated with statistical techniques. Only cohort studies were considered. The data reviewed show that platelet count, hematocrit, serum uric acid, and microalbuminuria are poor predictors of HDP. Mean arterial pressure predicts transient hypertension rather than preeclampsia. Fibronectin, urinary calcium excretion, roll-over test, and Doppler ultrasound showed contradictory and nonconclusive findings among the different authors. Isometric exercise test showed high predictive values but only two studies have been performed. Angiotensin II sensitivity was the test that showed the best predictive values but it is useless in clinical practice. In conclusion, currently, there is no test that fulfills all criteria established to be a good predictor of hypertensive disorders of pregnancy. The search for an adequate method for the screening of HDP with a high sensitivity, inexpensive, and easy to perform should still be a priority in future investigations.
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PMID:Evaluation of methods used in the prediction of hypertensive disorders of pregnancy. 816 16

Morphological examination of renal biopsies from 90 women with preeclampsia (PE), assessment of the clinical data and clinicomorphological correlations produced the following results: 1. By light-microscopy the renal lesions in PE imitate a picture of glomerulonephritis of mesangial type with different degrees of severity. 2. Morphometric investigations confirmed the impression gained by light-microscopy of swelling of endothelial cells and podocytes as well as endocapillary cell proliferation and enlargement of the glomeruli. 3. The immunohistological findings are non-specific and argue against immune complex deposition, but are suggestive of insudative processes. In addition immunohistological investigations of fibronectin and factor VIII-associated antigen reveal a pathogenetic relevant alteration of endothelial cell. 4. Electronmicroscopy is the most valid diagnostic method allowing subdivision of the quantitative different lesions in various degrees of severity. Furthermore the use of this method allows elucidation of the dynamics of the underlying disease process, which progresses through successive stages i.e. early, fully developed and late stage, supporting the reversibility of these glomerular lesions. 5. Close correlations are found between the clinical parameters and morphological findings in nephropathy in pregnancy-induced hypertension. The hypertension, proteinuria and nephrotic syndrome, which characterize the clinical picture, correlate with the severity of the glomerular lesions and the further course of the disease. Moreover, hypertension also correlates with mesangial and subendothelial deposits and with focal segmental hyalinosis and sclerosis, occurring in some cases. The focal segmental hyalinosis and sclerosis should be regarded as hyperperfusion-lesions indicating benign nephrosclerosis and developing only facultatively in PE. 6. The first morphological substrate of nephropathy in pregnancy-induced hypertension with the key to pathogenesis present itself as endothelial lesion, possibly caused by oxygen free radicals, lipid-peroxides or hyperfusion. In result of the endothelial lesion an imbalance of the different mediator systems i.e. thromboxane-prostacyclin, endothelin-EDRF with dominance of vasoconstrictive reactions would be effective. Thus the following induction of coagulative, vasoconstrictive and proliferative processes results in the characteristic glomerular lesions in PE.
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PMID:[Nephropathy in pregnancy--an endothelial lesion?]. 817 90

A large number of ascitic fluid tests, e.g., fibronectin and cholesterol, have been proposed as helpful in detecting malignancy as the cause of ascites. Unfortunately, these "humoral tests of malignancy" are nonspecific. Although the ascitic fluid concentrations of these proteins or protein-bound substances tend to be quite high in patients with peritoneal carcinomatosis and low in the setting of cirrhotic ascites, the problem is that patients with tuberculous peritonitis, cardiac ascites, pancreatitis ascites, etc. usually have values in the malignancy range, i.e., false-positive results. This can lead to an extensive search for a nonexistent tumor, with confusion and anxiety for patient and physician. The cytology is the single best test to order when peritoneal carcinomatosis is suspected; its sensitivity approaches 100%. However, peritoneal carcinomatosis is only one of several mechanisms by which tumors can cause ascites. No one test can be expected to detect tumors as the cause of these diverse mechanisms of ascites formation. The serum-ascites albumin gradient is a helpful test in classifying ascitic fluid specimens into portal-hypertension-related and non-portal-hypertension-related categories. An elevated serum alpha-fetoprotein test can be useful in raising suspicion of hepatocellular carcinoma. Careful analysis of ascitic fluid, without measurement of "humoral tests of malignancy," combined with information obtained from the history and physical examination, usually lead to an accurate diagnosis of the cause of ascites.
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PMID:Malignancy-related ascites and ascitic fluid "humoral tests of malignancy". 818 30

We performed these studies to assess the potential role of hemodynamic forces in mediating the changes in aortic fibronectin mRNA expression that occur in the rat in response to angiotensin II administration. With the use of an acute hypertensive model involving a 3-day infusion with a pressor dose of angiotensin II given by osmotic minipump, a selective increase in fibronectin mRNA expression but not of several other extracellular matrix genes was documented. This change was inhibited by losartan, indicating the importance of angiotensin receptors in the response. Prazosin, hydralazine, or L-arginine added to the drinking water all lowered the angiotensin II-induced increase in blood pressure but did not attenuate the increase in fibronectin mRNA expression. Angiotensin-converting enzyme inhibition using trandolapril did reduce fibronectin mRNA in the angiotensin II-infusion model, despite an inability to reduce blood pressure, whereas when angiotensin I was infused, quinapril lowered both blood pressure and fibronectin expression even at doses that did not completely normalize blood pressure. These studies suggest that angiotensin II induced an increase in aortic fibronectin mRNA that was not dependent solely on blood pressure.
Hypertension 1994 Jun
PMID:Angiotensin II alters aortic fibronectin independently of hypertension. 820 11

The aim of this study was to determine the phenotype of smooth muscle cells in the arteries of chronically hypertensive animals and to analyze the effects of treatments known to increase the survival of the animal without a clear effect on its hypertensive state. Stroke-prone spontaneously hypertensive rats (SHRSP) kept on a 1% sodium drinking solution were untreated or treated with one of two diuretics, indapamide (3 mg/kg per day) or hydrochlorothiazide (20 mg/kg per day), from 6 to 13 weeks of age. Phenotype was characterized by the immunolabeling of arteries with antibodies raised against a cellular form (EIIIA) of fibronectin, alpha-smooth muscle actin, and nonmuscle myosin. We demonstrated that phenotypes of smooth muscle cells of the SHRSP differ from those found in Wistar-Kyoto rats. The difference in phenotype is specific for the vessel type: ie, an increased expression of nonmuscle myosin in the aorta and of both EIIIA fibronectin and nonmuscle myosin in the coronary arteries. The two diuretics (1) had no effect on blood pressure, (2) prevented or did not prevent the increase in medial thickness, and (3) prevented changes in both smooth muscle cell phenotype and ischemic tissular lesions. Taken together, the results suggest that in SHRSP the changes in the phenotype of smooth muscle cells and the thickness of arteries are unrelated events. We propose that the maintenance of the contractile phenotype of the arterial smooth muscle cells could be an essential parameter involved in the prevention of the deleterious consequences characteristic of a severe hypertensive state.
Hypertension 1993 Nov
PMID:Arterial smooth muscle cell phenotype in stroke-prone spontaneously hypertensive rats. 822 26

A coarctation hypertensive rat model was used to examine the effects of elevated blood pressure on basement membrane component synthesis by cardiac myocytes and aorta using immunohistochemistry and Northern blot analysis. Carotid arterial pressure increased immediately on coarctation, and left ventricular hypertrophy was maximal within 5 days. In immunohistochemical studies, fibronectin and laminin were increased and the basement membrane chondroitin sulfate proteoglycan decreased in both the subendothelial space and smooth muscle cell basement membranes of the aorta above the clip compared with controls, whereas only fibronectin was elevated in the aorta below the clip. No change in basement membrane staining intensity for the cardiac myocytes was observed. Alterations in steady-state mRNA levels for fibronectin and laminin in the aorta paralleled those observed by immunohistochemical analysis with regard to protein and tissue type affected as well as intensity of the changes. However, changes in mRNA levels (but not protein deposition) for perlecan and type IV collagen were also observed in aortas from hypertensive rats compared with controls. Increases in steady-state mRNA levels for all basement membrane components in the heart and vasculature peaked before maximal cardiac hypertrophy (5 days). These studies indicate that alterations in basement membrane component deposition in the hypertrophied vasculature occur at both transcriptional and translational levels and suggest that the cell attachment glycoproteins fibronectin and laminin may be important factors in the vascular response to elevated transmural pressure.
Hypertension 1993 Nov
PMID:Coarctation induces alterations in basement membranes in the cardiovascular system. 822 34

To elucidate the mechanisms of hypertensive renal injury, we investigated the time course and extent of changes in matrix composition, as well as cell proliferation and infiltration in two-kidney, one clip rats. The nonclipped kidneys from hypertensive and sham-operated control rats (n = 5 to 10 in each group) were studied at 7, 14, 21, and 28 days after clipping. Systolic blood pressure was elevated by day 7 (154 +/- 3 versus 111 +/- 4 mm Hg in sham group, P < .001, n = 10 each). Hypertension resulted in an early expansion of the interstitial volume by 37%, whereas hypertensive vascular changes and glomerular injury did not become evident until day 21. Immunofluorescence studies revealed an early interstitial accumulation of collagens I, III, IV, V, VI, and fibronectin by day 7. In contrast, the glomeruli showed a mild to moderate increase in collagens I, III, IV, V, laminin, and fibronectin but not collagen VI later in the established phase of hypertension. Staining for proliferating cell nuclear antigen as a marker of cell replication was increased in tubular epithelial but not interstitial or glomerular cells. A progressive infiltration of macrophages (16 +/- 2 versus 9 +/- 1 ED1+ cells/mm2, P < .05, n = 6) and T lymphocytes (93 +/- 15 versus 74 +/- 7 CD4+ cells/mm2, n = 8) in the cortical interstitium had already occurred by day 7. On the other hand, only macrophages increased in number within the glomeruli. Thus, renovascular hypertension leads to an early tubular cell proliferation, mononuclear cell recruitment, and deposition of matrix proteins primarily within the interstitium. We conclude that the injury producing nephrosclerosis in this model extends far beyond the glomeruli. Both the tubules and the interstitium are actively involved and may be the more important initial sites of injury.
Hypertension 1993 Nov
PMID:Early interstitial changes in hypertension-induced renal injury. 822 35

Vascular endothelial cells are thought to play an important role in human aging as their senescence and detachment from a vascular wall may contribute to arteriosclerosis and high blood pressure in the elderly. We investigated the level of fibronectin (FN) expression in aortic endothelial cells aged in vivo, because FN is necessary for cell attachment and spreading and its increased expression had been shown in aging fibroblasts. The results showed that the steady state level of expression of FN mRNA increased with advancing donor age, while the labeling index of cultured cells decreased with age. Furthermore, the increased level of FN expression clearly correlated with an increase in cell area. In order to explore whether these changes reflected exhaustion of proliferation potential in vivo, we examined FN expression in human umbilical vein endothelial (HUVE) cells aging in vitro. Very similar results were obtained, supporting the idea that vascular endothelial cells age in vivo by using up division potential. Furthermore, we investigated the level of endothelin (ET) -1 mRNA expression during in vitro cellular aging of HUVE cells. The results showed that the expression of ET-1 gene was also up-regulated when the culture became old. It is very interesting that the genes for quite different proteins of FN and ET-1 are both up-regulated during cellular aging.
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PMID:Modulation of gene expression during aging of human vascular endothelial cells. 825 3

Hypertension produces myocyte hypertrophy and increases the extracellular matrix. In order to determine the composition of the extracellular matrix we studied the hearts from 14 hypertensive patients by immunohistochemistry using antibodies against collagen I, III, IV and V, fibronectin, myoglobin, muscular specific actin, Factor VIII, CD 34 and vimentin. The myocardium showed a focal increase in fibronectin, collagen I and III and diffuse deposition of laminin, collagen IV and V. Cells positive for vimentin, Factor VIII and CD 34 were also increased, but with considerable variation from case to case. We found no relation between matrix variation and the degree of hypertension or the time elapsed from the beginning of the disease. We conclude that the main role of the matrix in hypertension may be remodelling of the heart so that it entraps muscle fibres and increases their contractility.
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PMID:Alterations in the extracellular matrix of the myocardium in essential hypertension. 828 55

The 12-lipoxygenase pathway is a key mediator of angiotensin II (Ang II)-induced effects in the adrenal cortex. We also recently demonstrated that Ang II increases 12- and 15-lipoxygenase product levels in vascular smooth muscle cells. However, the relation between lipoxygenase activation and Ang II-induced vascular smooth muscle cell hypertrophy is not known. We studied the effects of Ang II and 12-lipoxygenase products on both total cell protein content and the levels of the matrix protein fibronectin in quiescent porcine aortic smooth muscle cells. Ang II-induced increases in cellular protein content were attenuated by the specific 12-lipoxygenase inhibitor baicalein; in contrast, the cyclooxygenase inhibitor ibuprofen had no effect. Direct addition of the 12-lipoxygenase product 12-S-hydroxyeicosatetraenoic acid increased total cell protein content. We have recently shown that porcine vascular smooth muscle cell growth is potentiated in high glucose (25 mmol/L) culture conditions. We observed that both Ang II and 12-S-hydroxyeicosatetraenoic acid induced a greater increase in protein content in cells cultured for two passages in high glucose. Furthermore, Ang II and 12-S-hydroxyeicosatetraenoic acid also markedly increased fibronectin levels in cells cultured in high glucose. These results suggest that 12-lipoxygenase activation plays a key role in Ang II-induced vascular smooth muscle cell hypertrophy. Furthermore, both Ang II and lipoxygenase effects are enhanced in cells cultured under hyperglycemic conditions.
Hypertension 1994 Jan
PMID:Role of the lipoxygenase pathway in angiotensin II-induced vascular smooth muscle cell hypertrophy. 828 45


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