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)

Captopril renin test (CRT) and captopril angioscintigraphic test (CAT) were simultaneously performed in 130 patients with arterial hypertension (72 women, 58 men, average age 48 years) and suspension for renovascular hypertension (RVH) in initial renal angioscintigraphy. 16 positive CAT results and 26 positive CRT results according to Muller qualification as well as 31 positive results according to Frederickson qualification were obtained. In 32 patients the suspension of RVH was formed on the basis of clinical features of accelerated phase of hypertension. In 42 patients the renal arteriography was performed-this group includes all patients with positive results of at least one captopril test, among them 32 patients with clinical symptoms of accelerated hypertension. In 24 cases the critical stenosis of renal artery was revealed. The diagnostic value of CRT-M, CRT-F and CAT was referred to critical stenosis of renal artery (> 75% of the lumen) as a criterium of RVH. The following values of sensitivity, specificity and discrimination capacity for CRT were established: for CRT-M 70%, 50%, 21% respectively, for CRT-F 88%, 44%, 40% respectively. CAT demonstrated the highest specificity (100%) as well as discrimination capacity (75%) in spite of the relatively low sensitivity (67%). The absence of false positive results of CAT as well as considerable percentage of false positive CRT results stress the importance of isotopic test as basic method for the diagnosis of RVH. Simplicity of the test, its low price and availability as well as immediately obtained results allow to propose CAT as a routine ambulatory screening test for RVH.
Pol Arch Med Wewn 1996 Mar
PMID:[Comparison of captopril angioscintigraphy and the renin test in diagnosis of renovascular hypertension]. 875 52

Neuropeptide Y (NPY) has been recently characterized as a circulating vasoconstrictor peptide which is co-stored with noradrenaline in sympathetic neurons. To investigate the role of NPY concentration in hypertension we measured the circulating NPY, endothelin-1,2 (ET-1,2), atrial natriuretic peptide (ANP), aldosterone, plasma renin activity (PRA) and noradrenaline (NA) in patients with stable mild to moderate primary hypertension. Circulating levels of NPY, ET-1,2, ANP, aldosterone and PRA were measured with radioimmunoassay, NA by double-isotope radioenzymatic assay. There were significant increase in concentrations NPY, ET-1,2, ANP and NA in patients with moderate primary hypertension, and significant positive correlations between the plasma levels of NPY, ET-1,2 and NA.
Pol Arch Med Wewn 1996 May
PMID:[Concentration of neuropeptide Y in serum of patients with primary hypertension]. 884 9

The relationship between sodium-sensitive hypertension, renin profile and genetic predisposition to hypertension have not been fully clarified. The present study aimed to establish the influence of family history of hypertension (at least one of the parents suffering from hypertension) on the renin profile, incidence of sodium-sensitivity of blood pressure and plasma concentration of selected biochemical parameters (creatinine, uric acid, glucose, sodium, potassium, calcium and cholesterol). 85 patients with essential hypertension (38 females, 47 males) were enrolled in the study. Secondary forms of hypertension were excluded in all patients by careful clinical and biochemical examination performed in the Department of Nephrology, Silesian University School of Medicine in Katowice. Plasma renin activity (PRA) was estimated twice: first after administration of a normal sodium diet (100-120 mmol of sodium per day) and 8 hours of supine position (PRA I) and a second time after 3 days of sodium restriction (10-20 mmol of sodium per day) and 3 hours of upright position (PRA II). All other biochemical parameters were measured once. Only patients with urinary sodium excretion lower than 60 mmol per day (after 3 days of low salt diet), were enrolled in the study. Sodium-sensitive hypertension was diagnosed in patients with a decrease of mean arterial blood pressure (MAP) of more or equal to 10 mm Hg after three days of sodium restriction. Reduction of MAP of less than 10 mm Hg was classified as sodium-nonsensitive hypertension. Among 85 patients with essential hypertension 49 (57.6%) had a positive (group I) while 36 (42.4%) a negative family history of hypertension (group II). Using the criteria presented in this study low, normal, high and rigid plasma renin activity were found, in 14.3%, 57.1%, 18.4% and 10.2% respectively of patients of group I. In patients of group II the incidence of the above mentioned renin profiles was similar: 13.9%, 58.3%, 19.4% and 8.4% respectively. In patients of group I 16 (32.7%) had sodium-sensitive and 33 (67.3%) sodium-nonsensitive hypertension, while in patients of group II 16 (44.4%) had sodium-sensitive and 20 (55.6%) sodium-nonsensitive hypertension (difference between group I and group II is statistically not significant). Patients of group I did not differ significantly from patients of group II with respect to : sex, age, blood pressure, sodium urinary excretion and plasma concentration of above mentioned parameters. From results obtained in this study we may conclude, that patients with and without history of essential hypertension do not differ with respect to renin plasma profile, incidence of sodium-sensitivity of blood pressure and other biochemical parameters.
Pol Arch Med Wewn 1996 Nov
PMID:[Renin plasma profile and sodium sensitivity of blood pressure in hypertensive patients with or without a family history of hypertension]. 909 55

Essential hypertension is a heterogenous multifactorial disease resulting from an interaction between genetic and environmental factors. Nature of genes responsible for the blood pressure regulation is not completely understood. Data from molecular biology studies with animals indicate that renin gene is involved in the pathogenesis of hypertension. Renin gene is one of the major candidate genes contributing to the pathogenesis of essential hypertension in humans. The aim of this study was the assessment of the association of RFLPs of human renin gene with essential hypertension in Polish population and search for the genetic marker of susceptibility to the disease. MspI, HindIII and EcoT141 RFLP in human renin gene locus were studied and polymorphic allele and genotype frequencies in the population of 74 hypertensive and 60 normotensive subjects were compared. MspI and HindIII RFLP analysis has not shown any statistically significant differences in allele and genotype frequencies between hypertensives and normotensives. These RFLPs do not seem to be in association with essential hypertension in studied population. EcoT141 RFLP analysis has not shown statistically significant differences in polymorphic alleles frequencies between examined groups. However, the observed difference between genotype E2O frequencies in hypertensives (0.31) and normotensives (0.12) was statistically significant (p < 0.045). A clinical importance of this finding is not known but genotype E2O seems to be a potential marker of susceptibility to essential hypertension. Further investigations in larger group of patients are required.
Pol Arch Med Wewn 1996 Aug
PMID:[Restriction fragment length polymorphism of human renin gene in essential hypertension]. 912 97

Our paper is discussing the presence and intensity of metabolic, humoral and haemodynamic abnormalities in mild middle-aged essential hypertensives (EH) and in hereditary predisposed still normotensive offspring from hypertensive families and their possible association with candidate genes changes. Four groups of subjects were compared (middle-aged normotensive controls (n = 21), corresponding patients with EH (n = 21), normotensive offspring from hypertensive (SH) (n = 56) and normotensive families (SN) (n = 56). Our results demonstrate that middle-aged patients with EH in our country have the same indices of hyperinsulinemia, impared glucose tolerance and insulin-sensitivity as previously described for other populations. They are accompanied by higher plasma concentrations of vasopressor substance like catecholamines, endothelin and lower levels of vasodepressor substances as ANP and kallikrein. The finding of similar, but quantitatively less expressed metabolic and humoral changes in SH but not in SN support the evidence for hereditary background of these abnormalities. The humoral and metabolic abnormalities may participate in BP elevation and in morphological and functional changes of left ventricle seen in SH (higher LV mass index, impaired diastolic filling). We did not prove an association between BP and polymorphism of ACE and angiotensinogen genes, however, our findings of association of DD genotype for ACE and M235 for angiotensinogen with higher insulinemia, plasma catecholamines and plasma renin activity evoke the hypothesis, whether the bearers of these genotypes, exposed for long-time to the higher concentrations of vascoactive substances, are not the subset of hereditary threatened subjects in whom clinically evident EH will manifest during their life.
Pol Arch Med Wewn 1997
PMID:Some metabolic, humoral and genetic aspects of arterial hypertension. 927 55

Serum levels endothelin-1,2 aldosterone, renin activity were performed in 52 patients with chronic congestive heart failure during captopril therapy. The investigations were done before therapy, after 10-15 days therapy and after disappearance symptoms of heart failure. The levels endotelin-1,2,aldosterone and renin activity were determined using radioimmunologic methods. Fraction ejection and peripheral vascular resistance were determined by echocardiography technics. It was found that serum endothelin levels in patients with chronic congestive heart failure were increased proportionally to functional class of heart failure and decreased after disappearance symptoms of heart failure. An increase in plasma endothelin concentration has not correlated with ejection fraction, aldosterone concentration and renin activity. These studies have demonstrated that in patients with congestive heart failure on captopril therapy endothelin serum levels positively correlates with peripheral vascular resistance. No correlation was found between ejection fraction and activity renin-angiotensin-aldosterone system. These findings indicated that captopril therapy decreases endothelin production.
Pol Merkur Lekarski 1997 Sep
PMID:[Does captopril decrease endothelial production of endothelin?]. 946 3

Nephropathy is a frequent complication of long term diabetes. Diabetic nephropathy is the major determinant of premature morbidity and mortality both in insulin-dependent (IDDM) and in non-insulin dependent-diabetes mellitus (NIDDM). There is good evidence that genetic predisposition plays a major role in development of diabetic nephropathy. This hypothesis is based on the observation that diabetic nephropathy clusters within families, both in IDDM and NIDDM. Components of the renin-angiotensin system (RAS) are plausible candidate genes to examine for a association with microalbuminuria and diabetic nephropathy. In this study we compared the distribution of PstI melting polymorphism at the ACE locus among NIDDM patients with diabetic nephropathy and in patients who, despite long duration of NIDDM, remain without this complication. The 220 NIDDM patients for whom DNA was available were classified into two groups according to their renal status: normoalbuminuric control subjects (n = 80) who are NIDDM patients with an A/C ratio < 2.5 and nephropathy cases (n = 140) who are NIDDM patients with A/C ratio > 2.5. Albumin excretion rate was assayed by radioimmunoassay. HbA1c was assayed using HPLC methods, creatinine--using Jaffe methods and DNA analysis using PCR reaction, and then after the amplification product was digested with PstI enzyme. The study revealed that PstI sequence differences ("+/= and -") in the ACE gene do not contribute to genetic susceptibility to diabetic nephropathy in NIDDM.
Pol Arch Med Wewn 1997 Jul
PMID:[Is PstI polymorphism of the angiotensin I converting enzyme gene associated with nephropathy development in non-insulin-dependent diabetes mellitus (preliminary study)]. 949 4

Endothelins (ETs) are peptides of 21 amino acids synthesized and released by variety of cells. Endothelin (now this peptide is called endothelin-1 (ET-1)) was isolated and identified in 1988 by Yanagisawa et al. Following studies revealed two other isoforms of endothelin': Endothelin-2 (ET-2) and endothelin-3 (ET-3). All of them bind to two types of receptors (A and B (ET-A r, ET-Br). ET-A r are responsible for concentration mediating. Two subtypes of ET-B r are known. ET-B1 r mediates vasorelaxation; ET-B2 vasoconstriction. ETs (especially ET-1) have variety of biological actions but the most important are vasoconstrictor and mitogenic action. Through these two mechanism ETs may participate in the pathogenesis and/or in the maintenance of hypertension in both experimental animal models and human essential hypertension. The intravenous infusion of synthetic ET induces a long-lasting elevation of blood pressure in experimental animals and in healthy humans. Number of studies have shown enhanced responses to ET in hypertensive subjects but decreased responses have also been reported. Similarly, plasma levels of ET-1 are either normal or elevated in experimental and human essential hypertension. Numerous investigators have suggested an interaction between ET and angiotensin-converting enzyme inhibitors through the renin-angiotensin system or through the accumulation of endogenous bradykinin. Also calcium antagonists of different classes prevent endothelin-induced contractions. Endothelin- converting enzyme inhibitor (phosphoramidon) and ET-A/B r antagonists (bosentan, BQ-123, FR139317) may have potential role as vasodilators in the treatment of hypertension.
Pol Merkur Lekarski 1998 Jan
PMID:[Endothelin and arterial hypertension]. 955 99

Angiotensin-converting enzyme (ACE) inhibitors are now established drugs in the treatment of hypertension and heart failure. The renin-angiotensin-aldosterone system is complex and acts as a circulating hormonal system, a local endogenous tissue system and neuromodular. Current experimental evidence suggests that ACE inhibitors reduce the risk associated with atherosclerotic cardiovascular disease. The antiatherogenic action of ACE inhibitors is related to complex effects mediated by these agent, including an antiproliferative and antimitotic action, beneficial effects on endothelial function, plaque-stabilizing effects and the action of these agents on the sympathetic nervous system. The role of ACE inhibitors in preventing the clinical sequale of atherosclerotic cardiac disease has been evaluated in various patient populations. Several small trial assess the effects of ACE inhibitors in severity of angina pectoris have reported conflicting results, with benefit is some patients and no benefit or even exacerbation of angina in others, indicating that ACE inhibitors do not have consistent antianginal effects in short-term study. ACE inhibitors have the theoretical potential to prevent restenosis after PTCA but they do not prevent restenosis and has no effect on overall clinical outcome. New data suggest that ACE inhibitors may be effective therapy fir patients following acute myocardial infarction. The renin-angiotensin system, is activated during new myocardial infarction and has an impact on the process of remodeling of the left ventricle which causes ist dysfunction and heart failure. In most of the large mortality trials the rationale for early treatment with ACE inhibitors after myocardial infarction was stated. ACE inhibitors have a positive effect in preventing the ventricular dilatation and they reduce the rate of reinfarctions and the mortality rate.
Pol Merkur Lekarski 1998 Jan
PMID:[The significance of converting enzyme inhibitor angiotensin I to angiotensin II in treatment of patients with coronary disease]. 955 7

Effects of cholecystokinin (CCK-33), caerulein (CER) and pentagastrin (PG) on arterial blood pressure and plasma renin activity (PRA) were studied in rats. The results showed that CCK-33 (106.25, 212.5 and 425.0 pmoles/kg i.v.) increased systolic and diastolic blood pressure and decreased PRA. CER used at doses: 0.37, 1.85 and 3.7 nmoles/kg (i.v.) did not change systolic blood pressure. CER administered at the higher doses slightly decreased diastolic blood pressure, evoked bradycardia and increased PRA. PG used at doses of 0.13, 1.3 and 13.0 nmoles/kg (i.v.) and the peptide given at the highest dose (13.0 nmoles/kg, i.v.) slightly increased arterial blood pressure. PG administered at all doses did not change PRA. This research shows that in spite of similarity in biochemical structure of CCK-33, CER, PG there are differences in effects of the studied peptides on arterial blood pressure and PRA. The correlation between an influence of CCK-33, CER and PG on arterial blood pressure and PRA was also observed.
Pol J Pharmacol
PMID:Effects of cholecystokinin, caerulein and pentagastrin on arterial blood pressure and plasma renin activity in rats. 956 45


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