Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reference values are usually based on blood samples from healthy men or non-pregnant women. Blood samples from pregnant women may be compared with these reference values. Correct references for pregnancy can be extremely important for clinical decisions such as ablatio placentae, appendicitis, premature rupture of membranes and preeclampsia. Previous studies of normal variations during third-trimester pregnancy are incomplete. Blood samples during pregnancy weeks 33, 36 and 39 as well as 1-3 h postpartum were collected from pregnant women with dietary iron supplement and at least one previous pregancy without a history of hypertension or preeclampsia. When the sampled values were compared with the present reference values from men and non-pregnant women, the following differences were found during normal pregnancy: Haemoglobin and ferritin were reduced, CRP was slightly elevated, WBC (white blood cell count) and HNL (human neutrophilic lipocalin) were elevated during pregnancy and significantly increased postpartum. Albumin was reduced. ALT and AST were slightly elevated and GGT was unchanged during pregnancy. ALP, D-dimer and fibrinogen were elevated. Uric acid increased during the third trimester and thrombocyte count decreased. Separate reference values for pregnant women are essential for correct diagnostic decisions during third-trimester pregnancy. Elevated levels of D-dimer do not necessarily indicate ablatio placentae. A diagnosis of progressive preeclampsia cannot be based on increasing uric acid levels and reduced platelet count in a stable clinical condition. HNL signals activation of neutrophilic granulocytes and can thereby offer a helpful tool for diagnosing infection during pregnancy and postpartum.
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PMID:New reference values for routine blood samples and human neutrophilic lipocalin during third-trimester pregnancy. 1176 17

Reported causes of pancreatitis in pregnancy include: gallstone disease, hyperlipidemia, alcohol ingestion, viral, and idiopathic. Few reports associate pancreatitis with pregnancy-induced hypertension. A 35-year-old women with pregnancy-induced hypertension and spontaneous rupture of membranes was admitted for induction of labor. Her postpartum course was complicated by acute renal failure that responded well to treatment with Lasix and Albumin. Subsequently, the patient developed acute pancreatitis and recovered following conservative treatment. It is possible that the pancreatic ischemia due to generalized vasoconstriction of preeclampsia and loop diuretics in the setting of oliguria with renal failure, had a synergistic effect on the pancreas. Therefore, we suggest that in postpartum women with pregnancy-induced hypertension and acute renal failure, diuretics should be cautiously used because they may increase the risk of pancreatitis.
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PMID:Pregnancy-induced hypertension complicated by postpartum renal failure and pancreatitis: a case report. 1201 78

Chronic diseases of the kidney have a progressive course toward organ failure. Common pathway mechanisms of progressive injury, irrespectively of the etiology of the underlying diseases, include glomerular capillary hypertension and enhanced passage of plasma proteins across the glomerular capillary barrier because of impaired permselective function. These changes are associated with podocyte injury and glomerular sclerosis. Direct evidence for causal roles is lacking, particularly for the link between intraglomerular protein deposition and sclerosing reaction. Because transforming growth factor-beta1 (TGF-beta1) is the putative central mediator of scarring, we hypothesized that TGF-beta1 can be up-regulated by protein overload of podocytes thereby contributing to sclerosis. In rats with renal mass reduction, protein accumulation in podocytes as a consequence of enhanced transcapillary passage preceded podocyte dedifferentiation and injury, increase in TGF-beta1 expression in podocytes, and TGF-beta1-dependent activation of mesangial cells. Angiotensin-converting enzyme inhibitor prevented both accumulation of plasma proteins and TGF-beta1 overexpression in podocytes and sclerosis. Albumin load on podocytes in vitro caused loss of the synaptopodin differentiation marker and enhanced TGF-beta1 mRNA and protein. Conditioned medium of albumin-stimulated podocytes induced a sclerosing phenotype in mesangial cells, an effect mimicked by TGF-beta1 and blocked by anti-TGF-beta1 antibodies. Thus, the passage of excess plasma proteins across the glomerular capillary wall is the trigger of podocyte dysfunction and of a TGF-beta1-mediated mechanism underlying sclerosis. Agents to reduce TGF-beta1, possibly combined with angiotensin blockade, should have priority in novel approaches to treatment of progressive nephropathies.
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PMID:Transforming growth factor-beta1 is up-regulated by podocytes in response to excess intraglomerular passage of proteins: a central pathway in progressive glomerulosclerosis. 1246 33

The aim of the work was to study the influence of pregnancy induced arterial hypertension (PIH) on hermetic aspects of the blood-brain barrier. Neurological consultation was followed by cranial computed tomography which revealed changes within structures of central nervous system. The observations were performed in 6 pregnant women, assigned to control group--C, and study group--G. All women had caesarean section performed in conductive anaesthesia. The method included collection of 15 ml venous blood and 4 ml cerebrospinal fluid (CSF). Albumin and immunoglobulin G (IgG) serum concentrations, micro-albumin and IgG CSF concentrations, and permeability indexes for albumin and IgG--Qalb and QIqG, were estimated. In contrast to group C, increased Qalb and QIgG indexes proved lack of integrity of blood-brain barrier in the group G. Control cranial CT scans revealed partial subsidence of changes after 3-5 days, and complete subsidence after 9-14 days.
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PMID:[Pregnancy induced arterial hypertension--an attempt to evaluate hermetic aspects of the blood-brain barrier connected with skull computed tomography]. 1263 19

The progression of renal disease correlates strongly with hypertension and the degree of proteinuria, suggesting a link between excessive Na+ reabsorption and exposure of the proximal tubule to protein. The present study investigated the effects of albumin on cell growth and Na+ uptake in primary cultures of human proximal tubule cells (PTC). Albumin (1.0 mg/ml) increased cell proliferation to 134.1 +/- 11.8% (P < 0.001) of control levels with no change in levels of apoptosis. Exposure to 0.1 and 1.0 mg/ml albumin increased total 22Na+ uptake to 119.1 +/- 6.3% (P = 0.005) and 115.6 +/- 5.3% (P < 0.006) of control levels, respectively, because of an increase in Na+/H+ exchanger isoform 3 (NHE3) activity. This was associated with an increase in NHE3 mRNA to 161.1 +/- 15.1% (P < 0.005) of control levels in response to 0.1 mg/ml albumin. Using confocal microscopy with a novel antibody raised against the predicted extracellular NH2 terminus of human NHE3, we observed in nonpermeabilized cells that exposure of PTC to albumin (0.1 and 1.0 mg/ml) increased NHE3 at the cell surface to 115.4 +/- 2.7% (P < 0.0005) and 122.4 +/- 3.7% (P < 0.0001) of control levels, respectively. This effect was paralleled by significant increases in NHE3 in the subplasmalemmal region as measured in permeabilized cells. These albumin-induced increases in expression and activity of NHE3 in PTC suggest a possible mechanism for Na+ retention in response to proteinuria.
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PMID:Effects of pathophysiological concentrations of albumin on NHE3 activity and cell proliferation in primary cultures of human proximal tubule cells. 1279 7

The question of whether influxes of ionic Ca+2 into cerebral endothelium plays an important role in increased vascular permeability consequent to an acute hypertension is not accurately resolved. We tested the effect of nifedipine, a calcium entry blocker, on the cerebrovascular permeability for proteins in adrenalin-induced acute hypertension. The experiments were carried out on male Wistar rats. The experimental groups consisted of normotensive saline controls, adrenaline-induced hypertensive rats, and adrenalin-induced hypertensive rats as pre-treated or post-treated with a bolus of nifedipine. Brains of hypertensive rats showed increased permeability to Evans Blue-Albumin complex, when blood pressure elevated rapidly to more than 170 mmHg. The number and size of areas of Evans-Blue extravasation were smaller if an increase in blood pressure was prevented. The short lasting elevation of blood pressure did not result in protein extravasation in brains of hypertensive rats. The results suggest that nifedipine can modify the permeability disruptions observed in acutely hypertensive rats. The data also support the hypothesis that Ca+2 may be responsible for the changes in permeability of BBB in hypertension by mediating the contraction of vascular muscles.
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PMID:Protection of blood-brain barrier breakdown by nifedipine in adrenaline-induced acute hypertension. 1519 55

The present study was undertaken to determine whether the severity of renal failure or hypertension in homozygous cyclooxygenase (COX)-2-deficient (COX-2-/-) mice affected by genetic background or gender. COX-2 deletion was introduced into three congenic genetic backgrounds, 129/Sv (129/COX-2-/-), C57/BL6 (C57/COX-2-/-), and BALB/c (BALB/COX-2-/-), by backcrossing the original mixed-background knockout mice with the respective inbred strains for 9 or 10 generations. Evaluation of the severity of hypertension and renal failure was performed in knockout and wild-type mice at the age of 2.5-3.5 mo. Blood pressure measured by tail-cuff plethysmography was significantly elevated in the male 129/COX-2-/- mice (165.8 +/- 9.2 vs. 116 +/- 5.1 mmHg, P < 0.05), and to a much lesser extent in the female 129/COX-2-/- mice (127.4 +/- 3.3 vs. 102.4 +/- 3.3), whereas it was unchanged in the C57- or BALB/COX-2-/- mice regardless of gender. Urinary excretion of albumin, determined by EIA, was remarkably increased in the 129/COX-2-/- (16.4 +/- 4.1 vs. 0.16 +/- 0.043 mg albumin/mg creatinine, P < 0.001), and to a lesser extent in the male C57/COX-2-/- mice (0.595 +/- 0.416 vs. 0.068 +/- 0.019). Albumin excretion was not elevated in the male BALB/COX-2-/- or in female COX-2-/- mice on any of the three genetic backgrounds. Histological analysis showed abundant protein casts, dilated tubules, and infiltration of inflammatory cells in the male 129/COX-2-/- mice, but not in COX-2-/- mice in other strains or gender. However, the presence of small glomeruli in the nephrogenic zone was observed in all strains of COX-2 knockout mice, regardless of genetic background and gender. Therefore, we conclude that the severity of hypertension and renal failure in COX-2-deficient mice is influenced by genetic background and gender, whereas the incomplete maturation of outer cortical nephrons appears to be independent of genetic background effects.
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PMID:Influence of genetic background and gender on hypertension and renal failure in COX-2-deficient mice. 1561 21

To prepare for shortage of blood components and to avoid side effects such as blood borne infectious disease, blood substitutes such as artificial red cell (artificial oxygen carrier) and artificial platelet are being developed. As for oxygen carriers, there are several candidates such as perfluorochemicals, modified hemoglobins and liposome encapsulated hemoglobins and albuimin heme. Perfluorochemicals have limited oxygen carrying capacity and oxygen inhalation is mandatory when they are used. Modified hemoglobins such as intermolecular or intramolecular cross linked hemoglobins have side effect to cause hypertension by scavenging nitro oxide (NO) which is produced by endothelial cells, because the size of these hemoglobins are small enough to go to the adjacent place near endothelial surface. Hemoglobin vesicles (HbV) in which hemoglobins are encapsulated in liposome is most possible candidate for oxygen carrier. Usefulness and safety of the HbV is evidenced by animal shock model or exchange transfusion model and they are now being prepared for clinical trials as red blood substitutes or oxygen therapeutics. Albumin heme in which recombinant human serum albumin incorporating synthetic heme is thought an ideal resuscitation fluid as this material has colloid oncotic pressure. Short time storage and viral infection are serious concern in platelet transfusion therapy for bleeding thrombocytopenic patients. Adhesion of the platelet to the collagen surface and aggregation at the bleeding sites to plug holes in blood vessels, and to facilitate the function of the remaining platelets is a starting point in developing platelet substitutes and several platelet substitutes have been proposed on this theory.
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PMID:[Artificial blood]. 1569 96

Management of hypertension and diabetes mellitus in primary health care requires occasional assessment of kidney function. Monitoring the urinary albumin excretion every 24 h is often used as a diagnostic gold standard but measurement of U-Albumin concentrations in morning urine either alone or together with U-Creatinine is a well-established surrogate measure. We compared the ratio U-Albumin/U-Creatinine and U-Albumin concentrations measured by commonly used POC (Point of care) instruments with those obtained in a central laboratory and estimated the uncertainty of the results after establishing an uncertainty budget. It is concluded that the presentation of ratios or concentrations on an ordinal scale is less satisfactory than reporting U-Albumin concentration on a ratio scale. Moreover the latter will have the advantage of allowing the physician to adjust the diagnostic sensitivity and specificity to local needs. The present report is a methodological study and does not consider the diagnostic performance of the studied properties per se.
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PMID:Are there advantages with U-Albumin/U-Creatinine ratios compared with U-Albumin in monitoring diabetes? 1617 75

One-quarter of adult population in different world regions are reported to live with hypertension, of whom, a high percentage had a diabetes mellitus (DM). This co-morbid state is believed to act synergistically on accelerating the long-term diabetic complications. Therefore, adequate treatment of high blood pressure is essential for diabetic patients, and should be always directed to their benefits. Albumin glycation is still the most important explanation for the pathogenesis of chronic diabetic complications. Our in vitro experiments induce non-enzymatic glycation of bovine serum albumin (BSA) under physiological conditions. The levels of advanced glycation end products (AGEs) were measured by their characteristic intrinsic fluorescence. Additions of captopril at concentrations from 5 to 50 microM caused 10-47% reduction in the formation of AGEs. Captopril binding properties of native and glycosylated BSA were characterized, and its affinity towards the native albumin was unaltered by the in vitro glycation. Therefore, we concluded that captopril could protect against albumin glycation, and it has a similar binding affinities towards native and glcosylated protein. Anti-glycation effect may help to attenuate the serious long-term diabetes related complications. Besides, the unchanged pharmacokinetic parameters provide an essential extra beneficial effect for diabetic hypertensive patients.
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PMID:Protective ability and binding affinity of captopril towards serum albumin in an in vitro glycation model of diabetes mellitus. 1646 67


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