Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the role of interleukin-6 (IL-6) in inflammatory disease we monitored plasma levels of IL-6 and acute phase proteins such as C-reactive protein (CRP) and renin substrate (RS) in patients with reactive arthritis (ReA), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). Venous plasma samples were collected: (1) during the acute phase or exacerbation of the disease, and (2) several months latter during convalescence. Increased mean [95% confidence intervals (CI)] levels of plasma IL-6 were observed in patients with ReA both in the acute phase and later, 229 (177 to 280) ng/l and 197 (134 to 260) ng/l respectively (P less than 0.001 as compared to controls). The corresponding plasma IL-6 levels in RA patients were 283 (223 to 340) ng/l and 183 (151 to 226) ng/l, respectively (P less than 0.001 as compared to controls). Plasma IL-6 levels in SLE patients were not increased. Plasma RS levels were increased in all patient groups, but no significant correlation to IL-6 or CRP levels was observed, whereas plasma IL-6 and CRP levels showed a positive correlation in ReA and RA patients.
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PMID:Plasma interleukin-6 and renin substrate in reactive arthritis, rheumatoid arthritis, and systemic lupus erythematosus. 138 3

The present study demonstrates that renal tubular unresponsiveness to aldosterone, without associated hyperkalaemia, is present in children with acute pyelonephritis. We studied 32 children with a diagnosis of acute pyelonephritis established by high fever, flank pain/tenderness, increased blood levels of C-reactive protein and significant Escherichia coli growth in the urine culture. Renal tubular function tests and determinations of plasma renin activity and aldosterone concentration were performed at diagnosis (study 1), after three days of iv gentamycin (study 2) and after 21 days of antibiotic therapy (study 3). Findings were compared to those present in 32 normal children of similar age. Despite normal plasma potassium concentration, fractional potassium excretion and transtubular potassium concentration gradient were significantly decreased in studies 1 and 2, becoming normal in study 3. Decreased renal potassium excretion coexisted with increased values for plasma renin activity and aldosterone concentration. In study 3 these hormones remained elevated only in patients with scarred kidneys. The functional alteration present in acute pyelonephritis may be directly caused by the interstitial inflammation or be mediated by some E. coli endotoxin.
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PMID:Normokalaemic pseudohypoaldosteronism is present in children with acute pyelonephritis. 149 6

We studied competitors in the 1983 Texan Challenge surf-ski paddle marathon to determine the effects of 4 days prolonged paddling on sweat rates, rectal temperatures, renal function, serum glucose, free fatty acid, porphyrin and C-reactive protein levels and serum creatine kinase activity. Sweat rates during the race varied from 0.5 to 1.0 l/h, and peak rectal temperatures did not exceed 38 degrees C, even in the most dehydrated subjects. Renal function was unchanged during the race. Plasma renin activity remained low during the race but C-reactive protein levels and serum creatine kinase activity were elevated. Seventy per cent of the subjects had immediate post-exercise blood glucose levels below 3.9 mmol/l after the 1st and 4th days, and 27% had values below 3.0 mmol/l, one competitor requiring intravenous glucose therapy on the beach. Surf-ski paddling is therefore associated with low sweat rates, low levels of dehydration, low body temperature and unchanged renal function. The low post-exercise blood glucose levels indicate that competitors must eat high-carbohydrate diets for the duration of the event and must either eat carbohydrate-containing foods or drink concentrated carbohydrate solutions while paddling.
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PMID:Physiological and biochemical measurements during a 4-day surf-ski marathon. 388 34

We hypothesized that increased levels of blood cytokines occur in brain-dead patients, and that these cytokines are responsible for some of the endocrine and/or acute-phase reactant abnormalities found in these patients. We measured blood levels of cytokines, hormones, and acute-phase reactants in 18 brain-dead potential organ donors at the moment of establishing the legal diagnosis of brain death and compared them with levels found in a control group. Although interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) levels were within the normal range, interleukin-6 (IL-6) levels were clearly above the normal range in all patients (median, 1,444 pg/mL; range, 75 to 11,780). In the brain-dead group, total thyroxine (tT4), free T4 (fT4), triiodothyronine (T3), thyrotropin (TSH), dehydroepiandrosterone sulfate (DHEA-S), testosterone, albumin, Zn, and osteocalcin levels were decreased, T3 resin uptake index (T3 RUI), corticotropin (ACTH), cortisol, 11-deoxycortisol (11-DOC), 17-hydroxyprogesterone (17-OHPr), aldosterone, luteinizing hormone, and follicle-stimulating hormone levels were normal, and reverse T3 (rT3), renin, and C-reactive protein (CRP) levels were increased. Multiple regression analysis demonstrated significant interrelations between IL-6 and T4, T3, testosterone, and CRP. We also studied the evolution of some of these parameters in four patients with severe head injury who finally developed brain death. IL-6 levels on admission to the intensive care unit (ICU) were above the normal limits, as in other patients with cranial trauma, but when the patients developed brain death, there was a pronounced increase in IL-6 levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood levels of cytokines in brain-dead patients: relationship with circulating hormones and acute-phase reactants. 754 Feb 49

A number of newer, "nontraditional" cardiovascular risk factors have been identified based on recent studies of the pathogenesis of atherosclerosis and atherothrombotic cardiovascular events. These include chronic inflammation and its markers, such as C-reactive protein; homocysteine; oxidative stress or endothelial dysfunction; lipoprotein Lp (a); psychosocial factors, such as environmental stress and responsiveness to stress; plasma insulin levels and markers of insulin resistance; and activation of the renin-angiotensin system, which is in part a function of polymorphisms in genes for components of the system, such as angiotensinogen and the angiotensin II type 1 receptor. The strength of the associations of the newer risk factors with cardiovascular therapy are currently being tested. This review will briefly discuss evidence that these risk factors are related to cardiovascular disease.
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PMID:Nontraditional cardiovascular risk factors. 1010 Jun 94

Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase), the rate-limiting enzyme of cholesterol synthesis. In recent years, statins have become the major choice of treatment for hypercholesterolemia. Emerging evidence from both animal and human studies indicates that mechanisms independent of cholesterol lowering effects contribute to the observed clinical benefits of statins. The anti-hypertrophy effect of statins on the cardiac tissue represents one of such mechanisms. The beneficial effects of statins on cardiac hypertrophy and cardioprotection may be attributed to their functional influences on small G proteins such as Ras and Rho, resulting in an increase of endogenous nitric oxide (NO), reduction of oxidative stress, inhibition of inflammatory reaction, and decrease of the renin-angiotensin system activity as well as C-reactive protein (CRP) levels in cardiac tissues. Recent findings from in vitro and in vivo studies of statins on cardioprotective effects are summarized in this review. The unveiled novel mechanisms support the use of statins as the new mainstay therapeutic agents for various cardiovascular diseases and complications.
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PMID:Perspectives on the cardioprotective effects of statins. 1287 Nov 30

We investigated the effects of pravastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, on interstitial inflammation and fibrosis, using an animal model of chronic cyclosporine A (CsA)-induced nephropathy. Sprague-Dawley rats were maintained on a low-salt diet (0.05% sodium) and treated daily for 1 or 4 wk with vehicle (olive oil; 1 ml/kg sc), CsA (15 mg/kg sc), or both CsA and pravastatin (5 or 20 mg/kg in the drinking water). Anti-inflammatory and antifibrotic effects of pravastatin were studied by evaluating the concentrations of the inflammatory mediators osteopontin (OPN) and C-reactive protein (CRP), of fibrotic cytokine-transforming growth factor (TGF)-beta1, and the presence of ED-1-positive cells (macrophages). In addition, renal function, serum lipid levels, histopathology (arteriolopathy and tubulointerstitial fibrosis), and the expression of the vasoactive factors endothelial nitric oxide synthase (eNOS) and renin protein were also compared for different treatment groups. Pravastatin induced dose-dependent decreases in the expression of OPN, intrarenal CRP, and TGF-beta1, and in the numbers of ED-1-positive cells at 1 and 4 wk. These were accompanied by a significant attenuation of tubulointerstitial fibrosis at 4 wk. The downregulation of eNOS protein expression in CsA-treated rat kidney was markedly upregulated by pravastatin treatment, although intrarenal renin expression was unaffected. Renal dysfunction induced by CsA significantly improved with administration of pravastatin at a dose of 20 mg/kg. Neither CsA nor pravastatin influenced serum lipid or high-sensitivity CRP levels in the treatment groups. Thus in chronic CsA nephropathy, pravastatin effectively abrogates the progression of tubulointerstitial inflammation and fibrosis. This may support the clinical use of pravastatin.
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PMID:Pravastatin treatment attenuates interstitial inflammation and fibrosis in a rat model of chronic cyclosporine-induced nephropathy. 1451 96

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are recognized primarily for their use in hypertension, in heart failure, and after myocardial infarction. New evidence, particularly with ACE inhibitors, has shown their ability to reduce acute coronary events associated with atherosclerosis in patients without a history of the aforementioned cardiac conditions. This is likely due to inhibitory effects on the renin-angiotensin system--a system that adversely influences fibrinolytic balance, vascular endothelial function, and vascular inflammation, all key components of atherosclerotic progression and adverse coronary outcomes. Results of various studies suggest favorable effects of ACE inhibitors and ARBs on markers of these components, including effects on plasminogen activator inhibitor-1, endothelin-1, and nitric oxide by ACE inhibitors, and effects on vascular cell adhesion molecule-1 and C-reactive protein by ARBs. Although early evidence suggests that ACE inhibitors may provide a greater beneficial effect on some of these markers compared with ARBs, and that certain ACE inhibitors may provide greater vascular benefits than others, further investigation is required to verify such findings. Overall, understanding the distinct coronary vascular benefits of these agents will emphasize the importance of using them, particularly ACE inhibitors, to improve outcomes in patients with coronary atherosclerotic disease.
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PMID:Pharmacologic blockade of the renin-angiotensin system: vascular benefits beyond commonly understood pharmacologic actions. 1452 46

The present study was designed to test the hypothesis that blockade of angiotensin II type-1 receptors reduces oxidative stress and inflammation in patients with essential hypertension. The study population comprised 132 hypertensive patients, some receiving and others not receiving medical treatment. At enrollment their systolic and/or diastolic blood pressures were > or = 140 and/or > or = 90 mmHg, respectively. The serum concentration of C-reactive protein, and the urine concentrations of 8-epi-prostaglandin F2alpha and 8-hydroxydeoxyguanosine were measured at baseline and after 12 weeks of treatment either with an angiotensin II type-1 receptor blocker, candesartan (8 mg daily) (age 64 +/- 12 years; male/female 28/39; n = 67), or other antihypertensive agents that do not block the renin-angiotensin system (age 65 +/- 10 years, male/female 25/40, n = 65). Candesartan reduced the levels of C-reactive protein (from 0.07 +/- 0.04 [median value +/- median absolute deviation] to 0.06 +/- 0.03 mg/dl, p < 0.0001), 8-epi-prostaglandin F2alpha (from 210 +/- 92 to 148 +/- 59 pg/mg creatinine, p < 0.0001), and 8-hydroxydeoxyguanosine (from 5.7 +/- 1.9 to 4.0 +/- 1.3 ng/mg creatinine, p < 0.0001), while the levels of these markers were not altered after the treatment with other antihypertensive agents. Blood pressure decreased by a similar amount in both groups, and the reductions in the levels of the markers did not correlate with that of blood pressure. These results suggest that candesartan reduces oxidative stress and inflammation in hypertensive patients independently of its effects on blood pressure. This may provide useful information for determining therapeutic strategies to minimize tissue injury by inflammation and oxidative stress in hypertensive patients.
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PMID:Candesartan reduces oxidative stress and inflammation in patients with essential hypertension. 1462 Sep 23

Cardiovascular disease, the most common cause of death in the Western world, results mainly from atherosclerotic remodeling of the arterial system. Atherosclerosis defines a disease in which the arterial wall becomes thickened and loses elasticity. This is clearly not a static condition. Instead, atherogenesis reflects a continuous development over time, ranging from macroscopically intact arteries to ruptured sclerotic plaques. Different stages at different sites can be present simultaneously within one individual. The pathophysiology of atherogenesis comprises various important steps, including enhanced endothelial permeability, expression of adhesion molecules, monocyte adhesion and immigration, foam cell formation, fatty streaks, smooth muscle cell migration and plaque formation, and, finally, plaque rupture and thrombus formation. In recent years, atherosclerosis is more and more being recognized as a chronic inflammatory process. The hypothesis of a chronic inflammation in atherosclerosis is supported by the following findings: atherosclerosis is associated with enhanced serum levels of inflammation parameters, including in particular C-reactive protein (CRP, Table 1); the atherosclerotic artery produces different hydrolytic enzymes, adhesion molecules, cytokines, and growth factors as seen in chronic inflammation; cells found in early atherosclerotic lesions are typically inflammatory cells (monocytes/ macrophages and T-lymphocytes); and, there is convincing clinical and experimental evidence that formation of reactive oxygen species (ROS) is augmented during this chronic inflammatory process due to an imbalance between synthesis of ROS and neutralizing antioxidative defense mechanisms. Studies in the general population could clearly show that markers of inflammation, in particular CRP, predict the cardiovascular risk. It is the aim of this review to discuss the role of inflammatory processes for the development of atherosclerosis and cardiovascular disease. Pro-inflammatory substances contributing to oxidative stress are listed in Table 2, and particular emphasis is placed on pathophysiologic effects induced by oxidized LDL and angiotensin II. Figure 1 summarizes important reaction steps of oxidative stress reactions, based on formation of superoxide anion (O(2)(-)). Finally, therapeutic options are presented, although it has to be emphasized that treatment with antibiotics proved to be essentially ineffective, and treatment options with antioxidants are not sufficiently evaluated to allow a final statement. Meanwhile, however, there is accumulating evidence that established treatment regimens with statins or renin-angiotensin system inhibitors possess profound anti-inflammatory and antioxidative properties which may support their beneficial effects on cardiovascular disease.
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PMID:[Atherosclerosis and arteriitis: implications for therapy of cardiovascular disease]. 1496 36


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