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)

Factor VII (FVII) is a plasma vitamin K-dependent glycoprotein that plays an important role in the initiation of tissue factor-induced coagulation (extrinsic pathway of blood coagulation). An increase in FVII coagulant activity (FVIIc) has been proposed as an independent risk factor for coronary artery disease. Recently, the coagulation assay using soluble tissue factor(sTF) enables us to measure the plasma levels of the activated form of factor VII(FVIIa) without the effect of the FVII zymogen form. We have developed the fluorogenic assay for FVIIa using sTF and measured the plasma FVIIa in atherosclerotic diseases. The FVIIa level in the Japanese was lower than that reported in Caucasians, suggesting that the incidence of ishemic heart disease is lower in the former. The FVIIa level was higher in the patients with cardiovascular diseases (ischemic heart disease and cerebral infarction), non-insulin-dependent diabetic mellitus, hypertension with microalbuminuria, and renal failure than in the healthy controls. The FVIIa levels were also increased in non-insulin-dependent diabetic patients, and this FVIIa increase was positively correlated with urinary albumin excretion. Furthermore, FVIIa levels were not correlated with the levels of lipids and the activity of hepatic synthesis, indicating that FVIIa may be an independent risk factor for cardiovascular disease.
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PMID:[Activated factor VII as a new cardiovascular risk factor of atherothrombotic disease]. 856 29

To learn more about the effects of ambient air pollution on the human immune system, immunological parameters-16 serum proteins and circulating immune complexes--were determined for more than 500 women from the polluted area of Cologne, Germany, and a control area, Borken. The geometric mean values for immunoglobulins, complement components, haptoglobin, alpha 1-acid glycoprotein, alpha 1-antitrypsin, ceruloplasmin, alpha 2-macroglobulin, prealbumin, and transferrin were statistically significantly higher in Cologne than in Borken. No difference were found for C-reactive protein, rheumatoid factors, and anti-streptolysin O. For each of the parameters a logistic regression was fitted, thus controlling for the influence of a number of confounding factors. After controlling for possible confounders, the percentages of values above the norm for immunoglobulins, complement components, haptoglobin, and alpha-1-glycoprotein were statistically significantly higher in Cologne than in Broken. Important confounders included overweight, high blood pressure, acute cold, fever in the preceding week, and smoking. The biochemical mechanisms underlying the observed interarea differences in protein profiles are as yet unknown and should be the subject of further, nonepidemiological research.
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PMID:Influence of air pollution on humoral immune response. 863 26

We investigated whether induced hypertension could enhance tumor uptake of monoclonal antibody. 111In-DTPA-A7 (IgG1 against 40kD tumor associated glycoprotein) was injected into colon carcinoma xenografted mice which were subcutaneously implanted with micro-osmotic pump containing angiotensin II (AT-II). Biodistribution was observed in groups of mice infused with AT-II at rate of 0.5 micrograms/kg/min (L) or 1 microgram/kg/min (H) and compared with a group of mice infused with saline (S). Tumor uptake of 111In-A7 in L and H was 1.32 and 1.57 times greater than S at 48 h after intravenous injection of A7. Normal organ uptakes also tended to be increased by AT-II infusion. Further study is needed to get optimum effect of hypertensive treatment on biodistribution of radiolabeled MoAb.
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PMID:Effect of induced hypertension with angiotensin II infusion on biodistribution of 111in-labeled monoclonal antibody. 886 85

Aortic dissection is not a popular disease but it should be listed in the disease to be excluded especially in acute emergent cases, because of its serious and protean clinical manifestations. While DeBakey classification was used over 30 years. Stanford classification is now widely accepted for its clinical availabilities. The features of the aortic dissection are 1) presence of the intimal tear at the proximal end in almost all cases, 2) its frequent location in the ascending aorta and aortic segment just distal to the left subclavian artery, and 3) the dissected plane at the outer media or medial-adventitial border. Systemic hypertension is frequently noticed in cases with aortic dissection. These features suggest hemodynamic effect as a pathogenic factor in addition to mural fragility of the aorta. Aortic dissection is frequently encountered in Marfan syndrome and other heritable diseases of connective tissue. Concerning Marfan syndrome, mutation of fibrillin gene was confirmed. Fibrillin is a microfibril consisting of glycoprotein closely bound to elastin. Therefore, traditional "cystic medial necrosis" which was referred as a principal morphological change corresponding to aortic dissection is now thought to be a secondary change to the aortic injuries occurred in the aortic wall.
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PMID:[Pathology of aortic dissection]. 896 88

High-affinity binding sites for the pancreatic beta-cell hormone amylin have been reported in the kidney, and it has been postulated that these sites may be involved in the genesis of hypertension. In the present study, we have used in vivo injection of 125I-amylin and in vitro autoradiographic techniques to assess renal amylin binding in both a genetic and a surgically induced model of hypertension. In the spontaneously hypertensive rat (SHR) at 6 weeks of age, before the rise in systolic blood pressure, there was a 36% increase in density of amylin binding compared with their normotensive counterpart, the Wistar-Kyoto rat (WKY). In SHR, there was a further increase in the density of amylin binding (to 53% greater) as the systolic blood pressure rose between 6 and 12 weeks of age. Histological examination of kidneys from SHR at 12 weeks of age revealed staining for a brush border glycoprotein, normally restricted to the proximal tubules, extending from the urinary pole into half of the epithelial lining of the glomerular capsule. In contrast to WKY, these cells also bound 125I-amylin with high density in SHR. In a rat model of renal ablation and hypertension, systolic blood pressure correlated with the density of 125I-amylin binding in the renal cortex (r=.54, P=.003, n=28). The changes in amylin binding reported here suggest a possible role for this peptide and/or activation of its receptor in the genesis as well as the maintenance of hypertension.
Hypertension 1997 Sep
PMID:Increased density of renal amylin binding sites in experimental hypertension. 931 32

Non-insulin-dependent diabetes mellitus (NIDDM) is commonly associated with hypertriglyceridaemia, low serum HDL-cholesterol concentrations, hypertension, obesity and accelerated atherosclerosis (metabolic syndrome X). Since a similar dyslipidaemia occurs with the acute-phase response, we investigated whether elevated acute-phase/stress reactants (the innate immune system's response to environmental stress) and their major cytokine mediator (interleukin-6, IL-6) are associated with NIDDM and syndrome X, and may thus provide a unifying pathophysiological mechanism for these conditions. Two groups of Caucasian subjects with NIDDM were studied. Those with any 4 or 5 features of syndrome X (n = 19) were compared with a group with 0 or 1 feature of syndrome X (n = 25) but similar age, sex distribution, diabetes duration, glycaemic control and diabetes treatment. Healthy non-diabetic subjects of comparable age and sex acted as controls. Overnight urinary albumin excretion rate, a risk factor for cardiovascular disease, was also assayed in subjects to assess its relationship to the acute-phase response. Serum sialic acid was confirmed as a marker of the acute-phase response since serum concentrations were significantly related to established acute-phase proteins such as alpha-1 acid glycoprotein (r = 0.82, p < 0.0001). There was a significant graded increase of serum sialic acid, alpha-1 acid glycoprotein, IL-6 and urinary albumin excretion rate amongst the three groups, with the lowest levels in non-diabetic subjects, intermediate levels in NIDDM patients without syndrome X and highest levels in NIDDM patients with syndrome X. C-reactive protein and cortisol levels were also higher in syndrome X-positive compared to X-negative patients and serum amyloid A was higher in both diabetic groups than in the control group. We conclude that NIDDM is associated with an elevated acute-phase response, particularly in those with features of syndrome X. Abnormalities of the innate immune system may be a contributor to the hypertriglyceridaemia, low HDL cholesterol, hypertension, glucose intolerance, insulin resistance and accelerated atherosclerosis of NIDDM. Microalbuminuria may be a component of the acute-phase response.
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PMID:NIDDM as a disease of the innate immune system: association of acute-phase reactants and interleukin-6 with metabolic syndrome X. 2212 8

Angiotensin II (ANG II) has been implicated in the hypertrophic and fibrotic responses of the heart and kidney to systemic hypertension. To determine whether these actions of ANG II are related to tissue-specific stimulation of growth factors, we infused adult Sprague-Dawley rats with ANG II at 50 ng/min (low dose), 100 ng/min (high dose), or vehicle for 1 week. Rats receiving vehicle or low-dose ANG II were normotensive with normal plasma aldosterone concentration, whereas rats receiving high-dose ANG II were hypertensive with increased plasma aldosterone. Tissue fibrosis was quantified morphometrically, and messenger RNA (mRNA) for transforming growth factor-beta1 (TGF-beta1) and prepro-epidermal growth factor (EGF) was measured in liver, heart, and renal glomeruli and tubules. In addition, mRNA was determined for clusterin, a glycoprotein expressed in response to tissue injury. Compared to vehicle, low-dose ANG II increased TGF-beta1 expression in glomeruli, tubules, and heart, but not in liver, and increased EGF expression in renal tubules only. High-dose ANG II decreased clusterin expression in liver only. Fibrosis was induced by low- and high-dose ANG II in kidney and heart, but not in liver. We conclude that ANG II selectively stimulates TGF-beta1 mRNA in the heart and kidney, which may contribute to cardiac and renal interstitial fibrosis resulting from activation of the renin-angiotensin system independent of hypertension. By stimulating cellular proliferation, selective stimulation by ANG II of EGF in renal tubules may amplify the effects of TGF-beta1. Suppression of clusterin expression in the liver of hypertensive rats may represent a specific response to high levels of circulating ANG II or a response to hypertensive injury.
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PMID:Tissue-specific regulation of growth factors and clusterin by angiotensin II. 965 31

Tamm-Horsfall protein (THP) is a glycoprotein that is exclusively produced by the kidney in the thick ascending limb of Henle's loop (TAHL). Disturbances of TAHL function are associated with decreased urinary THP excretion. It is well known that renal function declines with advancing age. Moreover, it is suggested that THP may play a role in the pathophysiology of hypertension. The aim of this study was to assess urinary excretion of THP (U-THP) in healthy and hypertensive elderly patients. Fifteen young healthy subjects (YHS), 15 young hypertensive patients (YHT), 15 older normotensive (>60 years) subjects (OHS) and 31 older (>60 years) hypertensive patients (OHT) were examined. In all subjects 24-h urinary volume (UV), U-THP and creatinine (U-Cr), specific gravity of urine (U-SG), serum creatinine (S-Cr), and mean arterial pressure (MAP) were assessed. THP urinary excretion was significantly decreased in normotensive elderly patients, but not in hypertensive ones. Higher U-THP in the elderly hypertensive as compared with the elderly normotensive patients seems to be more the consequence than the cause of arterial hypertension.
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PMID:Urinary excretion of Tamm-Horsfall protein in normotensive and hypertensive elderly patients. 978 95

Type II (non-insulin-dependent) diabetes mellitus is associated with increased blood concentrations of markers of the acute-phase response, including sialic acid, alpha-1 acid glycoprotein, serum amyloid A, C-reactive protein and cortisol, and the main cytokine mediator of the response, interleukin-6. The dyslipidaemia common in Type II diabetes (hypertriglyceridaemia and low serum levels of HDL cholesterol) is also a feature of natural and experimental acute-phase reactions. We review evidence that a long-term cytokine-mediated acute-phase reaction occurs in Type II diabetes and is part of a wide-ranging innate immune response. Through the action of cytokines on the brain, liver, endothelium, adipose tissue and elsewhere, this process could be a major contributor to the biochemical and clinical features of metabolic syndrome X (glucose intolerance, dyslipidaemia, insulin resistance, hypertension, central obesity, accelerated atherosclerosis) but also provides a mechanism for many other abnormalities seen in Type II diabetes, including those in blood clotting, the reproductive system, metal ion metabolism, psychological behaviour and capillary permeability. In the short-term, the innate immune system restores homeostasis after environmental threats; we suggest that in Type II diabetes and impaired glucose tolerance long-term lifestyle and environmental stimulants, probably in those with an innately hypersensitive acute-phase response, produce disease instead of repair.
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PMID:Is type II diabetes mellitus a disease of the innate immune system? 1023 Jun 57

Prior to 1972, the increased cardiovascular morbidity and mortality that diabetics endure had been attributed to vascular disease. In 1972, Rubler et al. proposed the existence of a diabetic cardiomyopathy based on their expereince with four adult diabetic patients who suffered from congestive heart failure (CHF) in the absence of discernable coronary artery disease, valvular or congenital heart disease, hypertension, or alcoholism. Alternative explanations for CHF, such as anemia and vascular and renal disease in these four patients, gave rise to criticisms, but a wave of subsequent studies in the 1970s and 1980s provided credence to this new disease entity. This review of the studies done since 1972 appears to support the concept of a diabetic cardiomyopathy independent of atherosclerotic cardiovascular disease. The exact mechanism is still questionable, and several mechanisms have been proposed including small and microvascular disease, autonomic dysfunction, metabolic derangements, and interstitial fibrosis. However, the weight of evidence leans toward the development of fibrosis, possibly caused by the accumulation of a peroxidase acid schiff (PAS)-positive glycoprotein, leading to myocardial hypertrophy and diastolic dysfunction.
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PMID:Diabetic cardiomyopathy. 985 79


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