Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
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Inflammatory processes are increasingly recognized as important participants in the pathophysiology of hypertension and cardiovascular disease. Angiotensin II may be to a large degree responsible for triggering vascular inflammation by inducing oxidative stress, resulting in up-regulation of inflammatory mediators. Inflammatory markers such as C-reactive protein are increased in the blood of patients with hypertension and predict the development of cardiovascular disease. Moreover, C-reactive protein may be a pro-inflammatory molecule under certain circumstances. C-reactive protein and high blood pressure in combination have additional predictive value for cardiovascular outcomes, as they contribute as independent determinants of cardiovascular risk. Therapeutic intervention aimed to reduce vascular inflammation in hypertensive patients has been proposed. Recent lines of evidence suggest that lifestyle modification and pharmacological approaches may reduce blood pressure and inflammation in patients with hypertension. Antagonism of the renin-angiotensin system with the selective angiotensin receptor blockers may improve cardiovascular outcome beyond blood pressure control, by reducing vascular inflammation and remodeling.
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PMID:Reduction of C-reactive protein and the use of anti-hypertensives. 1820 Aug 16

Children of parents with hypertension are at increased risk of developing high blood pressure. We hypothesize that circulating concentrations of putative biomarkers (that may play a role in development of high blood pressure) are higher in nonhypertensive offspring of parents with hypertension. We compared concentrations of 4 different biomarkers (urinary albumin:creatinine ratio, circulating C-reactive protein, aldosterone:renin ratio, and plasminogen activator inhibitor-1) in nonhypertensive Framingham offspring study participants with none (n=233), 1 (n=474), or both (n=322) parents with hypertension. Parental hypertension was defined as onset before age 60 years, based on longitudinal observations of the original Framingham cohort. Serum C-reactive protein concentrations were higher in nonhypertensive offspring with 1 (median: 1.7; Q1 to Q3: 0.8 to 3.6 mg/L) or both parents with hypertension (median: 1.8; Q1 to Q3: 0.7 to 3.6 mg/L) compared with offspring without parental hypertension (median: 1.4; Q1 to Q3: 0.7 to 3.2 mg/L). In multivariable analyses, parental hypertension was associated with higher serum C-reactive protein concentration in offspring (15% increase per parent with hypertension; P=0.004). Prospectively, the relation of parental hypertension to longitudinal changes in blood pressure in the nonhypertensive offspring was attenuated on adjustment for C-reactive protein (P=0.04 for attenuation). The levels of the other biomarkers evaluated did not significantly differ in offspring according to parental hypertension status. In conclusion, serum C-reactive protein concentrations are higher in nonhypertensive offspring of parents with hypertension. These data suggest that inflammation may partly mediate the familial influences on hypertension risk.
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PMID:Association of parental hypertension with concentrations of select biomarkers in nonhypertensive offspring. 1857 71

Inflammation is an important factor in the development and progression of atherosclerosis. Observational studies have suggested that renin-angiotensin system inhibition might lower C-reactive protein (CRP). The aim of this study was to test the hypothesis that angiotensin-converting enzyme inhibition with fosinopril would reduce inflammation in a placebo-controlled trial involving 621 subjects. CRP was determined using a high-sensitivity assay at baseline and after 3 months of fosinopril treatment. The median CRP level at baseline was 1.38 mg/dl (interquartile range 0.64 to 2.86) and did not significantly differ between treatment groups. CRP levels at baseline were significantly associated with future cardiovascular events, even after adjustment for age and gender (odds ratio 1.76, 95% confidence interval 1.16 to 2.67, p = 0.008). Fosinopril treatment during 3 months did not result in a significantly higher reduction of CRP levels compared with placebo (difference -0.11, p = 0.20). Exploratory analysis suggested an interaction between gender and fosinopril treatment on CRP reduction (p = 0.07). Male gender was associated with a significantly larger reduction in CRP compared to female gender. In conclusion, contrary to previous observational studies, no effect of angiotensin-converting enzyme inhibition on CRP levels was found.
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PMID:Effect of fosinopril treatment on serum C-reactive protein levels in patients with microalbuminuria. 1860 26

A calcium channel blocker (CCB), azelnidipine (AZ), is reported to inhibit oxidative stresses, particularly when administered under blockade of the renin-angiotensin system (RAS). The purpose of this study was to investigate whether AZ inhibits oxidative stresses more potently than other CCBs under blockade of RAS and exerts renoprotection in type 2 diabetic nephropathy. Subjects were hypertensive type 2 diabetics with nephropathy, taking RAS inhibitors. The patients were randomly assigned to two groups, an AZ group (n=21, 16 mg/d) and a nifedipine-CR (NF) group (n=17, 40 mg/d). The plasma levels of monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), high-sensitive C-reactive protein (hsCRP), adiponectin and tumor necrosis factor-alpha (TNF(alpha)), the urinary excretion of 8-epi-prostaglandin F(2alpha) (8-epi-PGF(2alpha)) and 8-hydroxydeoxyguanosine (8-OHdG), and the urinary albumin-to-creatinine ratios (ACR) were determined before and after 16-week treatment. Neither metabolic parameters nor blood pressure levels differed between the two groups not only at baseline but also after the treatment. However, significant decreases in MCP-1, IL-6, hsCRP, TNF(alpha), 8-epi-PGF(2alpha), 8-OHdG and ACR levels, and a significant increase in the plasma adiponectin level were detected in the AZ group, but not in the NF group. The % change in the urinary oxidative stress markers correlated with that in ACR. Our results indicate that, in hypertensive patients with diabetic nephropathy, a combination therapy of RAS inhibitors and AZ is an effective therapeutic modality for decreasing not only blood pressure but also inflammations and oxidative stresses.
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PMID:Combination therapy with renin-angiotensin system inhibitors and the calcium channel blocker azelnidipine decreases plasma inflammatory markers and urinary oxidative stress markers in patients with diabetic nephropathy. 1871 62

Genetic factors have been shown to influence high-sensitivity C-reactive protein (hsCRP) levels, however, which genes that are involved in this process remains to be clarified. The renin-angiotensin system (RAS) is of importance for the regulation of inflammation, and blockade of angiotensin II type 1 receptors (AGTR1) influences hsCRP levels. These findings prompted us to investigate whether a polymorphism in the AGTR1 gene may influence hsCRP levels. Additionally, a polymorphism in the CRP gene that has previously been shown to influence hsCRP levels was genotyped. Serum levels of hsCRP were measured in 270 42-year-old women recruited from the population registry. Two single nucleotide polymorphisms were analysed: +1166A>C and +1444C>T of the AGTR1 and CRP gene, respectively. The A allele of the AGTR1 polymorphism +1166A>C was dose-dependently associated with higher hsCRP levels (p=0.014, adjusted for confounding factors and multiple comparisons). hsCRP levels were not significantly influenced by the CRP +1444C>T genotype; however, an interaction between the two studied polymorphisms with respect to hsCRP levels was observed (p=0.018). The significant association between the AGTR1 polymorphism and hsCRP levels, which appears to be independent of anthropometric and metabolic traits, is yet another indication of a direct influence of RAS on inflammation.
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PMID:Association between the AGTR1 polymorphism +1166A>C and serum levels of high-sensitivity C-reactive protein. 1902 96

Although the list of clinical complications associated with HIV therapy continues to grow, the underlying mechanisms remain incompletely understood. Metabolic abnormalities, such as dyslipidaemia, insulin resistance and cardiovascular disease continue to top the list, but there is an increasing appreciation of the effect of HIV and antiretroviral therapy on body composition, bone metabolism, muscle function and autonomic nervous system control of lipid and glucose metabolism. The 10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV brought together physicians and researchers in the area of HIV management with world experts involved in adipose tissue metabolism and lipid regulation, bone and muscle metabolism and renin-angiotensin and blood pressure control to review and discuss recent findings in these areas. The data presented at the meeting highlight that studies of adipose tissue remain a major focus of attempts to unravel the pathophysiology that accompany lipodystrophy associated with HIV infection and/ or its therapy. There is also a growing appreciation and understanding of the direct role of HIV in the development of various comorbidities, including bone disease, cardiac dysfunction and neuropathologies, including peripheral neuropathy. Two key emerging themes were those of mitochondrial dysfunction and a heightened basal inflammatory state, exemplified by increased levels of proinflammatory cytokines, chemokines and markers such as C-reactive protein. These might prove to be the common denominators that link HIV-associated pathologies with diverse organ systems.
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PMID:Key data from the 10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV, 6-8 November 2008, London, UK. 1919 38

1. Inhibiting the renin-angiotensin-aldosterone system prevents left ventricular (LV) remodelling after myocardial infarction (MI). 2. The present study was designed to assess the effects of a combination of perindopril and losartan on LV remodelling, cardiac function and serum procollagen type III amino terminal peptide (PIIINP) levels in patients with acute MI. 3. Patients with anterior MI were divided into three groups: (i) MI + perindopril; (ii) MI + losartan; and (iii) MI + perindopril + losartan. After successful intervention therapy, perindopril (2-4 mg daily), losartan potassium (25-50 mg daily) or their combination were administered. All patients received aspirin, clopidogrel and statins, and some patients were given beta-blockers, nitrate and a platelet glycoprotein IIb/IIIa receptor antagonist. Three months later, LV dimensions and LV ejection fraction (LVEF) were measured by ultrasonography. Plasma B-type natriuretic peptide (BNP), serum C-reactive protein (CRP) and PIIINP levels were evaluated using enzyme-linked immunosorbent assay or radioimmunoassay. 4. The baseline characteristics of the three groups were the same. Three months after the initiation of therapy, all patients showed decreased CRP, increased BNP and PIIINP levels and LV dilation and dysfunction. Compared with the two monotherapy groups, patients in the combination group showed significantly lower CRP, BNP and PIIINP levels, less LV dilation and higher LVEF. Serum PIIINP levels were positively correlated with CRP levels (r = 0.597; P < 0.01) and LV end-diastolic volume index (r = 0.543; P < 0.01) and were negatively correlated with LVEF (r = -0.565; P < 0.01). 5. For patients with acute MI, combination treatment with perindopril and losartan significantly inhibited LV remodelling and improved LV function. Inhibition of myocardial interstitial fibrosis may be part of the underlying mechanism.
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PMID:Effects of combination therapy with perindopril and losartan on left ventricular remodelling in patients with myocardial infarction. 1920 20

Osteoprotegerin (OPG), a member of tumor necrosis factor receptor superfamily, has been implicated in vascular disease. We investigated the association of serum OPG with the ankle-brachial index (ABI) and urine albumin:creatinine ratio (UACR), in a bi-ethnic cohort of 1324 African-Americans (mean age 64 years, 71% women) and 1237 non-Hispanic whites (mean age 59 years, 57% women) belonging to hypertensive sibships. Serum levels of OPG were measured by solid phase sandwich immunoassay. ABI was measured using a standard protocol and peripheral arterial disease (PAD) defined as ABI<0.90. UACR was expressed as mg albumin/gm creatinine. Multivariable regression analysis using generalized estimating equations (GEE) were performed to assess whether serum OPG levels were associated with ABI and UACR. After adjustment for conventional risk factors (age, sex, diabetes, waist circumference, history of smoking, total and HDL cholesterol, hypertension), prior history of myocardial infarction or stroke, and medication (renin-angiotensin-aldosterone system inhibitors, statins, aspirin, estrogen) use, higher OPG levels were significantly associated with lower ABI and higher UACR in African-Americans (P=0.001 and P<0.0001, respectively) and non-Hispanic whites (P=0.017 and P=0.002, respectively); the association remained significant after further adjustment for plasma C-reactive protein (CRP) in both ethnic groups. In multivariable logistic regression analysis, higher OPG levels were associated with PAD in African-Americans, independent of the covariates listed above (P=0.026); the association remained significant after additional adjustment for plasma CRP (P=0.047). In non-Hispanic whites, the association of higher OPG levels with PAD was of borderline significance after adjustment for the relevant covariates (P=0.106). We conclude that higher OPG levels are associated with lower ABI and higher UACR, independent of conventional risk factors and plasma CRP.
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PMID:Association of serum osteoprotegerin with ankle-brachial index and urine albumin: creatinine ratio in African-Americans and non-Hispanic whites. 1942 12

Congestive heart failure (CHF) is the main cause of acute dyspnea in patients presented to an emergency department (ED), and it is associated with high morbidity and mortality. B-type natriuretic peptide (BNP) is a polypeptide, released by ventricular myocytes directly proportional to wall tension, for lowering renin-angiotensin-aldosterone activation. For diagnosing CHF, both BNP and the biologically inactive NT-proBNP have similar accuracy. Threshold values are higher in elderly population, and in patients with renal dysfunction. They might have also a prognostic value. Studies demonstrated that the use of BNP or NT-proBNP in dyspneic patients early in the ED reduced the time to discharge, total treatment cost. BNP and NT-proBNP should be available in every ED 24 hours a day, because literature strongly suggests the beneficial impact of an early appropriate diagnosis and treatment in dyspneic patients.Etiologic diagnosis of febrile patients who present to an ED is complex and sometimes difficult. However, new evidence showed that there are interventions (including early appropriate antibiotics), which could reduce mortality rate in patients with sepsis. For diagnosing sepsis, procalcitonin (PCT) is more accurate than C-reactive protein. Thus, because of its excellent specificity and positive predictive value, an elevated PCT concentration (higher than 0.5 ng/mL) indicates ongoing and potentially severe systemic infection, which needs early antibiotics (e.g. meningitis). In lower respiratory tract infections, CAP or COPD exacerbation, PCT guidance reduced total antibiotic exposure and/or antibiotic treatment duration.
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PMID:Useulness of B Natriuretic Peptides and Procalcitonin in Emergency Medicine. 1957 5

Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. The understanding of the pathophysiology of AF has changed during the last several decades, and a significant role of inflammation and of the renin-angiotensin-aldosterone system has been postulated both experimentally and clinically. There is emerging evidence of an association between inflammation and AF, and mounting evidence links increased C-reactive protein levels not only to already existing AF but also to the risk of developing future AF. The beneficial effects of statins on AF have been reported in several studies. Several randomized clinical and large observational studies have shown similar result that show the beneficial effect of statins in AF. In clinical studies, statins were considered effective in preventing AF after electrical cardioversion, post-ablation, and after permanent pacemaker and implantable cardioverter defibrillator insertion. The antiarrhythmic mechanisms of statins regarding AF prevention in patients with heart failure are still not clear. Perioperative statin use has been associated with favorable postoperative outcome in both cardiovascular and noncardiovascular conditions. Despite a growing body of evidence that drugs with anti-inflammatory properties such as statins may prevent AF, the observed positive effects of statins on the burden of AF appeared to be independent of their cholesterol-reducing properties. However, further data from large-scale randomized trials are clearly needed.
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PMID:Pleiotropic effects of statins in atrial fibrillation patients: the evidence. 1959 May 88


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