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)

Diabetic nephropathy is the most frequent cause of end-stage renal failure. One of the crucial factors in a development of renal and cardiovascular complications of diabetes is genetic predisposition. The genes of the renin-angiotensin system are important group of candidate genes involved in pathogenesis of chronic renal diseases. The purpose of our study was the evaluation of a possible role of genetic polymorphisms of some of the RAS system genes in the nephropathy in type 2 diabetes. The study was performed in 117 patients with diabetic nephropathy, compared with 200 healthy subjects as a control group. The following polymorphisms: insertion/deletion (I/D) of the angiotensin-converting enzyme gene (ACE), M235T of the angiotensinogen gene (AGT) and A1166C of the angiotensin II type 1 receptor gene (AT1R) were evaluated by polymerase chain reaction (PCR). No statistically significant differences between groups were found in the allele frequency and genotype distribution for ACE and AGT polymorphisms. The results for the AT1R gene polymorphism revealed significant differences in allele and genotype frequencies. The homozygous CC genotype was more frequent in patients with diabetic nephropathy than in control group. Both genotypes with the C allele (AC + CC) were found in 56% of patients compared to 38% in control group. These results suggest increased susceptibility to diabetic nephropathy in individuals carrying the CC genotype. Therefore, the A1166C polymorphism of the AT1R gene could be a potential genetic marker for increased susceptibility to renal complications in type 2 diabetes.
Pol Arch Med Wewn 2002 Aug
PMID:[Association of the renin-angiotensin system gene polymorphism with nephropathy in type II diabetes]. 1247 91

The renin-angiotensin-aldosterone system plays an important role in the regulation of electrolyte balance, body fluid volume and blood pressure. As yet, angiotensin II has been ascribed actions mediated by first type of receptors (AT1) such as increased blood pressure, antinatriuretic effect, cell proliferation. Since several years studies have been conducted on the role of second type receptor (AT2) through which angiotensin manifests its effects opposing those resulting from stimulation of type 1 receptor. They include: release of bradykinin and nitric oxide, vasodilation, natriuretic and antiproliferative effects. Blockade of the function of this receptor causes excessive reaction induced by action exerted on AT1 receptor.
Pol Merkur Lekarski 2003 Feb
PMID:[Unexpected properties of angiotensin mediated by the AT2 receptor: possible therapeutic implications]. 1272 64

Chronic heart failure (CHF) constitutes a significant clinical issue due to its increasing prevalence in general population and still fatal prognosis. During last twenty years the significance of beta-blockers in the treatment of CHF has changed. It resulted from the hypothesis from 1975 that in the course of CHF it comes to the activation of sympathetic system and renin-angiotensin-aldosterone system. Authors presented the actual views on CHF pathogenesis, mechanisms of favourable action of beta-blockers in CHF and the data from clinical trials on effectiveness of beta-blockers in different stages of CHF (among the others in elderly patients and in comparison with other treatment). Nevertheless, there are still several questions related to beta-blockers treatment in patients with CHF waiting to be resolved. Although the number of patients with CHF treated with beta-blockers is still increasing, the usefulness of conclusions resulting from clinical trials--as it has been shown in IMPROVEMENT-HF--is still insufficient. In contrast, following the recommendations of ESC, AHA and the Section of Heart Failure of Polish Cardiology Association both beta-blockers and ACE inhibitors constitute two main groups of medications that should be undoubtedly used in patients with CHF.
Pol Merkur Lekarski 2003 Apr
PMID:[Beta-blockers in chronic heart failure]. 1286 3

Vasovagal syncope is defined as a reflex loss of consciousness related to reaction to various stimuli as orthostatic stress, pain or emotions connected with loss of muscle postural tone. The aetiology of this disorder is still unknown. The imbalance between the parts of autonomic nervous system and other homeostasis-related systems as renin-angiotensin-aldosterone system, peptides as endothelin, neuropeptide Y, vasopressin, adrenomedullin and cAMP, adenosine and AMP can play an important role in the development of vasovagal syncope. In the first part of the paper the authors describe the mechanisms involved in the development of vasovagal reaction, pathophysiology of the head-up tilt test and the role of autonomic nervous system.
Pol Merkur Lekarski 2003 Apr
PMID:[Neurohumoral mechanisms for vasovagal syncopes. Part I]. 1286 5

The inhibitory effect of lipopolysaccharides (LPS) on alpha-adrenergic contraction is quite well known, but molecular mechanism of this inhibition is unclear. In the present study, the interaction between alpha-adrenoceptor and vasopressin receptor response, and LPS in rat tail artery was investigated using chemical stimulation. In the presence of LPS, noradrenaline, phenylephrine and arginine-vasopressin, concentration-response curves (CRCs) were shifted to the right with the change in maximal responses. The K(A) and K(B) values calculated in the presence and absence of LPS did not differ significantly. The results strongly suggest that LPS did not change the receptors affinity. The changes in the relationship between receptor occupancy and response to an agonist in the presence of LPS and reduction of K(A)/ED(50) value suggest reduction of receptor reserve. In the presence of angiotensin II (Ang II), CRCs were shifted to the right with significant increase in receptor reserve. Moreover, this effect was still present in LPS-pretreated arteries. The receptor reserve reduced by LPS significantly increased in the presence of Ang II. It suggests that inhibitory effect of LPS is partially reversible. The results strongly suggest that in early endotoxemia, inhibitory effect of LPS may by partially reverted by an increase in activity of renin-angiotensin-aldosterone system.
Pol J Pharmacol
PMID:Physiological antagonism of angiotensin II and lipopolysaccharides in early endotoxemia: pharmacometric analysis. 1470 72

Essential hypertension accounts for 95% of all cases of hypertension. A small number of patients (between 2% and 5%) have a reversible disease as the cause for raised blood pressure. Unilateral and bilateral renal artery stenosis may be responsible for secondary hypertension. Diagnosis and treatment of renal artery stenosis are of a great importance. Revascularization of ischemic kidney may correct blood pressure control and preserve renal function. Much data suggest close pathophysiological relation between renal artery stenosis, ischemic nephropathy and development of hypertension. However, it should be stressed that not every renal artery stenosis leads to hypertension and ischemic nephropathy. Therefore diagnosis of renal artery stenosis in hypertensive patient is not always equivalent with renovascular hypertension. The true prevalence of renal artery stenosis is unknown. In unselected population it accounts for less than 1% of hypertensive patients. Renovascular etiology of hypertension may be suggested by abrupt onset of hypertension, resistant and malignant hypertension or recurrent pulmonary edema of unknown etiology. Physical examination may reveal bruits over major vessels, including the abdominal aorta and renal arteries. The principle aim of the renal artery stenosis investigation is to confirm presence and size of vessel obstruction and its association with hypertension. Typical evaluation is based on imaging techniques and physiological studies. Former include: doppler duplex ultrasonography, conventional angiography, intraarterial and intravenous digital subtraction angiography, computed axial tomography, magnetic resonance angiography and intravascular ultrasonography. Functional studies are occasionally used. These are renal scintigraphy, evaluation of plasma renin activity in renal veins and evaluation of plasma rennin activity after ACE inhibition. Treatment of patients with renal artery stenosis and hypertension should restore vessel patency and inhibit its occlusion. Revascularization should elicit an improvement in or normalization of blood pressure control and renal function. Therapeutic approach include percutaneous renal artery angioplasty (PTRA), with or without stenting, revascularization by surgery and pharmacotherapy. PTRA is currently the first choice option. In general, it is simpler and similarly effective as surgical reconstruction. In some cases PTRA is completed with stent placement. It prevents immediate recoil but does not completely eliminate restenosis of revascularized artery. Surgical bypass is currently reserved for patients in whom PTRA and stenting fail and in patients with extensive atherosclerotic lesions. Patients with renal artery stenosis and hypertension should be provided with pharmacological treatment according to current recommendations. Specific procedures to limit associated risk factors of atherosclerosis should also be introduced.
Pol Merkur Lekarski 2003 Oct
PMID:[Renovascular hypertension: is it only the top of the iceberg?]. 1497 69

The effect of angiotensin II antagonist, losartan, on chronic stress-induced elevation of blood glucose levels was investigated in rats. Chronic immobilization stress caused an increase in blood glucose levels in rats. Administration of losartan (3 mg/kg, po) before stress exposure significantly prevented this increment. We suggest that losartan showed this effect by decreasing the excessive sympathetic response to stress. In conclusion, there is a relationship between stress, sympathetic nervous system, and renin-angiotensin system.
Pol J Pharmacol
PMID:Losartan may prevent the elevation of plasma glucose levels induced by chronic stress. 1515 79

The T(-344)C polymorphism in promoter of CYP11B2 gene encoding aldosterone synthase has been associated with differences in plasma aldosterone (ALDO) concentrations. In addition, the results of recent study carried out in Japan suggest that C(-344) allele of CYP11B2 may be a genetic marker of salt-sensitive hypertension characterized by low plasma renin activity (PRA) and high ALDO/PRA ratio. Therefore, it raises the question of whether the T(-344)C polymorphism of CYP11B2 gene may be associated with salt-sensitive hypertension in Caucasians. The DNA samples were obtained from 68 Polish hypertensives. During 3 subsequent 1-week periods each subject received diets of normal, low and high sodium content (120-140, 20-40 and 240-260 mmol Na+/day, respectively). Salt sensitivity was expressed as the difference between mean arterial pressure (MAP) on high salt diet and MAP on low salt one (delta MAPH-L). Genomic DNA isolated from peripheral blood nuclear cells was amplified by PCR method with primers flanking the polymorphic region and C(-344) allele was identified by gain of Hae III restriction site. There were 14 TT homozygotes (20.6%), 35 TC heterozygotes (51.5%) and 19 CC homozygotes (27.9%) in the studied group. No significant differences in delta MAPH-L, glomerular filtration rate, natriuresis, excreted fraction of filtered sodium, PRA, ALDO and ALDO/PRA ratio determined on each diet have been found in subjects according to CYP11B2 genotype. Our preliminary results suggest the lack of association of the T(-344)C CYP11B2 polymorphism with salt-sensitive hypertension as well as with activity of plasma renin-angiotensin-aldosterone system in Caucasian patients.
Pol Arch Med Wewn 2004 Feb
PMID:[Promoter variants of aldosterone synthase gene (CYP11B2) and salt-sensitivity of blood pressure]. 1523 Feb 31

A high-performance liquid chromatographic assay has been developed to the separation of angiotensin I, tetradecapeptide and the tetrapeptide Leu-Val-Tyr-Ser. This purpose is achieved in a single step, using HPLC technique in the reversed phase system. The method is based on enzymatic hydrolysis of a substrate renin (TDP) with formation of angiotensin I (DP). After 1 h incubation at 37 degrees C the reaction mixture is introduced directly into the chromatographic system. A 200 microl reaction mixture is needed for analysis. Acetonitrile gradient in 0.01 M ammonium acetate buffer allows a satisfactory separation of hydrolysis products. The application of this technique for the determination of in vitro renin activity and evaluation the potency of human renin inhibitors, employing the artificial renin substrate tetradecapeptide, is demonstrated.
Acta Pol Pharm
PMID:Determination of in vitro activity renin inhibitors by HPLC method. 1548 Dec 40

Bartter syndrome is an uncommon tubular disorder inherited as an autosomal recessive entity. It is associated with hypokalemic metabolic alkalosis with high renin and aldosterone plasma concentration with low or normal blood pressure. Recent studies have demonstrated genetic heterogeneity in Bartter syndrome. Mutations of two genes encoding the Na/K/2Cl cotransporter and potassium channel ROMK are responsible for clinical features of neonatal Bartter syndrome. Mutations of gen encoding the chloride channel ClC-Kb is identified as being causative for the classic Bartter syndrome. And dysfunction of Na/Cl cotransporter in the distal convoluted renal tubule is described as Gitelman syndrome.
Pol Merkur Lekarski 2004 May
PMID:[Bartter's syndrome]. 1551 34


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