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)

Hypertension is the major risk factor for coronary heart disease, stroke, and renal disease. Also, it is probably the most important risk factor for peripheral vascular disease and vascular dementia. Although hypertension occurs in both men and women, gender differences have been observed. However, whether sex hormones are responsible for the observed gender-associated differences in arterial blood pressure, and which is their mechanism of action, remains unclear. Local and circulating renin-angiotensin systems (RAS) are examples of systems that may be involved in the pathogenesis of hypertension. Classically, angiotensin II (Ang II) has been considered as the effector peptide of the RAS, but Ang II is not the only active peptide. Several of its degradation products, including angiotensin III (Ang III) and angiotensin IV (Ang IV) also possess biological functions. These peptides are formed via the activity of several aminopeptidases. This review will briefly summarize what is known about gender differences in RAS-regulating aminopeptidase activities, their relationship with sex hormones, and their potential role in controlling blood pressure acting through local and circulating RAS.
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PMID:Hypertension, RAS, and gender: what is the role of aminopeptidases? 1821 72

Pharmacological inhibition of the renin-angiotensin-aldosteron system (RAAS) constitutes a cornerstone strategy in the management of patients with chronic nephropaties and proteinuria. Angiotensin converting enzyme inhibitors (ACEI) as well as angiotensin II subtype 1 receptor antagonists (ARA) have been shown to decrease proteinuria, reduce the local renal inflammatory processes and slow the progression of renal insufficiency. Despite recent progress, there is still no optimal therapy which inhibits progression of renal disease. It is possible that pentoxifilline (PTX) an old medication which is still used to treat peripheral vascular disease will be the new adjunct to RAAS blockade. In addition, PTX has been shown to decrease the production of pro inflammatory cytokines and reactive oxygen species. 61-Year-old man with nephrotic proteinuria, diabetes type 2, hypertension, chronic viral hepatitis type C and slightly impaired renal function was desribed. Proteinuria as daily urine protein excretion (DPE), serum creatinine and eGFR (MDRD mode) were measured. Proteinuria was diagnosed in 2003 (DPE 3.5 g), creatinine 1.3-1.5 mg/dl. The patient had been examined in Department of Nephrology but exact reason of nephrotic syndrome was not recognized because he refused kidney biopsy. Therapy was started with ACEI and temporary effect as decrease of DPE to 0.2 g, eGFR was about 60 ml/min. and serum creatinine in normal range. In 2004 DPE increased to 8.98-9.42 g, serum creatinine 1.1-1.3 mg/dl. The dose of ACEI was increased and after then ARA was added. After one month of combined therapy DPE fell to 7.7 g, next the doses of both drugs were increased to maximum (losartan 100 mg and lisinopril 40 mg) and DPE fell to 6.8 g, serum creatinine was 1.4 mg/dl and potassium 5.4 mmol/l. Next PTF 800 mg/day was added and DPE fell to 0.55 g after 2 months' therapy. Similar DPE was after 6 months (0.53 g) since we started with combination of IKA, ARA and PTF.
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PMID:[Clinical state of a patient with nephrotic proteinuria successfully treated with combined therapy with angiotensin II receptor antagonists and angiotensin II converting enzyme inhibitors and pentoxifylline]. 1885 64

Pharmacological inhibition of the renin-angiotensin-aldosteron system (RAAS) constitutes a cornerstone strategy in the management of patients with chronic nephropathies with proteinuria and with chronic renal failure. Angiotensin converting enzyme inhibitors (ACEI) as well as angiotensin II subtype 1 receptor antagonists have been shown to decrease proteinuria, reduce the local renal inflammatory processes and slow the progression of renal insufficiency. Despite recent progress, there is still no optimal therapy that would stop progression of renal disease. May be pentoxifilline (PTF)--the old medication which is still used to treat peripheral vascular disease and brain ischemia will be the new adjunct to RAAS blockade. In addition, PTF has been shown to decrease the production of pro-inflammatory cytokines and reactive oxygen species. PTF therapy may improve the hemoglobin response in patients with previously rh-EPO resistant anemia in renal failure. This may occur due to inhibition of proinflammatory cytokine production. Probably in the next few years we will get answer to the question of PTF role in nephrology.
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PMID:[Pentoxifylline old drug or new hope for nephrology?]. 1900 36

Hypertension, a multifactorial-polygenic disease, interacts with multiple environmental stressors and results in functional and structural changes in numerous end organs, including the cardiovascular system. This can result in coronary heart disease, stroke, peripheral vascular disease, congestive heart failure, end-stage renal disease, insulin resistance, and damage to the pancreatic islet. Hypertension is the most important modifiable risk factor for major health problems encountered in clinical practice. Whereas hypertension was once thought to be a medical condition based on discrete blood pressure readings, a new concept has emerged defining hypertension as part of a complex and progressive metabolic and cardiovascular disease, an important part of a cardiometabolic syndrome. The central role of insulin resistance, oxidative stress, endothelial dysfunction, metabolic signaling defects within tissues, and the role of enhanced tissue renin-angiotensin-aldosterone system activity as it relates to hypertension and type 2 diabetes mellitus are emphasized. Additionally, this review focuses on the effect of hypertension on functional and structural changes associated with the vulnerable pancreatic islet. Various classes of antihypertensive drugs are reviewed, especially their roles in delaying or preventing damage to the vulnerable pancreatic islet, and thus delaying the development of type 2 diabetes mellitus.
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PMID:Treating hypertension while protecting the vulnerable islet in the cardiometabolic syndrome. 2040 6

Agents that block the renin-angiotensin system (RAS), including angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, are of proven benefit in patients after ST-segment elevation myocardial infarction (STEMI). However, no studies have evaluated the benefit of pre-event use of RAS inhibitors before STEMI. A retrospective review was performed of patients admitted to a single hospital with the diagnosis of STEMI and without a history of coronary disease or the equivalent, including diabetes mellitus, peripheral vascular disease, or stroke. Patients were stratified according to the use of RAS inhibitors before STEMI. Compared to patients not taking RAS inhibitors, patients who were taking RAS inhibitors had a lower peak troponin I level (79 vs 120 ng/dl, p = 0.016). Of the patients who had medically treated hypertension, those receiving RAS inhibitors had a significantly lower peak troponin I compared to those receiving non-RAS agents (79 vs 130 ng/dl, p = 0.015), despite equivalent blood pressure across the 2 groups. The beneficial effect of RAS inhibitor pretreatment remained when concomitant aspirin and statin use were controlled for. In conclusion, in patients presenting with a first STEMI, pretreatment with RAS inhibitors conferred a cardioprotective effect. The mechanism of this benefit appears to be independent of an effect on blood pressure control and was not wholly due to the effect of concomitant use of other medicines known to be protective in patients with STEMI.
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PMID:Relation of pre-event use of inhibitors of the renin-angiotensin system with myocardial infarct size in patients presenting with a first ST-segment elevation myocardial infarction. 2072 39

Angiographic imaging in 1986 employs not only conventional film arteriography and venography, but also digital subtraction angiography (DSA). Arteriography is still the best method of demonstrating pathology in patients with peripheral vascular disease. Transluminal angioplasty, its indications and results are discussed. Patients with suspected renovascular hypertension should be given intravenous DSA and, if pathology is demonstrated, renin sampling as well. Patients with severe, acute, life-threatening hemorrhage may have angiography not only to localize bleeding sites, but also to treat them by transcatheter embolization techniques. Various other angiographic techniques including venous sampling are discussed briefly.
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PMID:Angiographic imaging. 2126 4

Essential hypertension is one of the major contributors to premature morbidity and mortality due to the incresased risk for coronary heart disease, stroke, renal disease, peripheral vascular disease and vascular dementia for both men and women. However, its basic causes remain unknown. In the present work we studied the activity of several proteolytic regulatory enzymes related to renin-angiotensin-system (RAS) (aminopeptidase A, APA; aminopeptidase N, APN; aminopeptidase B, APB; and insulin-regulated aminopeptidase, IRAP); with oxytocin regulation (oxytocinase); with the metabolism of GnRH and TRH (pyrrolidone carboxypeptidase, Pcp); and with enkephalins metabolism (enkephalindegrading activity, EDA), to elucidate their role in the mechanisms responsible of essential hypertension and to discuss the possible gender differences. Serum samples of 53 individuals with essential hypertension and 60 healthy volunteers were collected and used to assay enzyme activities, gonad hormones testosterone and estradiol, TSH and free thyroxin (fT4). Differences were observed in APA, APN, Pcp and EDA specific activities, and in serum gonad hormone levels between hypertensive and control groups. Only Pcp activity showed gender differences. Regarding the RAS, APA is reduced while APN is increased, suggesting increased levels of angiotensin II and a facilitation of the conversion of angiotensin III in angiotensin IV. Thus, the changes in several RAS-regulating specific activities and other enzyme activities involved in the neuroendocrine modulation of gonad and stress-related functions are related to essential hypertension with minor gender differences. Therefore, aminopeptidases constitute new elements for the knowledge of the causes of essential hypertension and an alternative as therapeutic targets against the illness.
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PMID:Circulating aminopeptidase activities in men and women with essential hypertension. 2393 Dec 76

Renal artery stenosis especially that due to atherosclerotic peripheral vascular disease is increasing in the population. The role of the renin angiotensin aldosterone system in the pathogenesis of renovascular hypertension is widely accepted. There is increasing recognition of the role of the sympathetic nervous system, from both afferent and efferent signaling pathways, as a contributor to development of hypertension. In this review we briefly summarize the experimental evidence for the respective roles of the renin angiotensin aldosterone system and the sympathetic nervous system as well as their interaction in renovascular hypertension.
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PMID:Interactions between the sympathetic nervous system and angiotensin system in renovascular hypertension. 2397 94

Vitamin D deficiency is a condition that affects a high percentage of individuals of all ages. Considerable attention has been paid recently to the possible role of deficiency of this vitamin in the development of several chronic diseases, including cardiovascular and metabolic diseases. In particular, vitamin D deficiency is associated with an increase in conditions such as obesity, insulin-resistance, hypertension, diabetes, and an increased risk of death from these pathologies. There is also a significant correlation with mortality for major cardiovascular events such as heart failure, myocardial infarction, sudden cardiac death, stroke, atrial fibrillation, and peripheral vascular disease. The pathophysiological mechanisms of these correlations are yet to be determined, but hyperactivity of the renin-angiotensin-aldosterone system seems to play a leading role. The role of therapy with vitamin D supplements in improving cardiovascular outcome in patients with low levels of vitamin D remains to be determined.
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PMID:[Vitamin D deficiency and cardiovascular diseases]. 2568 47

Hypertension is a major public health problem in the developing as well as in developed countries due to its high prevalence and its association with coronary heart disease, renal disease, stroke, peripheral vascular disease, and related disorders. Essential hypertension (EH) is the most common diagnosis in this disease, suggesting that a monocausal etiology has not been identified. However, a number of risk factors associated with EH have also been identified such as age, sex, demographic, environmental, genetic, and vascular factors. Recent advances in molecular biological research had achieved clarifying the molecular basis of Mendelian hypertensive disorders. Molecular genetic studies have now identified mutations in several genes that cause Mendelian forms of hypertension in humans. However, none of the single genetic variants has emerged from linkage or association analyses as consistently related to the blood pressure level in every sample and in all populations. Besides, a number of polymorphisms in candidate genes have been associated with differences in blood pressure. The most prominent candidate has been the polymorphisms in the renin-angiotensin-aldosterone system. In total, EH is likely to be a polygenic disorder that results from inheritance of a number of susceptibility genes and involves multiple environmental determinants. These determinants complicate the study of blood pressure variations in the general population. The complex nature of the hypertension phenotype makes large-scale studies indispensable, when screening of familial and genetic factors was intended. In this review, recent genetic studies exploring the molecular basis of EH, including different molecular pathways, are highlighted.
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PMID:Molecular genetics of essential hypertension. 2702 74


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