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)

Hearts of 50 patients (males of 30 to 54 years) after sudden cardiac death (SCD) without myocardial infarction, acute or recorded in the past, were studied. Heart slides were stained with an iron hematoxylin; polarizing microscopy was also used. The surface of cardiomyocytes diffusely stained with an iron hematoxylin was determined in histological slides by means of a 100-points ocular mesh. Essential differences in the spread of contractural myocardial lesions were found, this likely to be bound with different mechanisms of death (ventricular fibrillation, asystole). A low degree of spread of these lesions was noted more frequently in grave stenoses (greater than 75%) of coronary arteries. A direct correlation between the spread of contractural lesions and renin activity in plasma is found.
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PMID:[Atherosclerotic stenosis of the coronary arteries and contraction lesions of the myocardium in sudden coronary death]. 389 Aug 7

In idiopathic haemochromatosis, excessive iron deposits include adrenal cortex, and mainly the zona glomerulosa. In this view, we measured basal and post-stimulative values of plasma cortisol, aldosterone and renin activity (RA) in two groups of patients: 1) 9 normal-salt repleted subjects (NSR) who were subjected to iv ACTH and furosemide tests, 2) 10 patients who were subjected to chronic salt depletion (CSD), to iv ACTH and furosemide tests. The results were compared with two groups of 7 healthy volunteers (NSR and CSD). In the patients, basal cortisol values were either normal or increased in cases of poorly controlled diabetes (21 +/- 2.1 microgram/100 ml, P < 0.01) and cortisol increase after ACTH injection was normal (to 43.3 +/- 4.3 microgram/100 ml). In the 9 NSR patients, basal aldosterone (7.75 +/- 1.5 ng/100 ml) and RA (1.55 +/- 0.27 ng/ml/h) values were normal; aldosterone and RA rose after furosemide injection: these increases were similar in these patients (respectively to: 13.5 +/- 2.2 ng/100 ml and 4.3 +/- 0.6 ng/ml/h) and in the 7 NSR controls. In the 10 CSD patients, basal aldosterone and RA values were always increased (26.5 +/- 3.2 ng/100 ml and 8.5 +/- 2.3 ng/ml/h) as much as in the 7 CSD controls. After ACTH administration, aldosterone values (26.1 +/- 4 in NSR patients, 54 +/- 8 ng/100 ml in CSD patients) were the same as in the two control groups. This study suggests that there is no adrenocortical deficiency in idiopathic haemochromatosis, in spite of excessive iron deposits in the adrenal cortex.
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PMID:Adrenocortical function in idiopathic haemochromatosis. 625 7

Weanling rats were fed a casein-based diet containing either 150 ppm cadmium, 500 ppm nickel, or the combination of these metals for 16 wk. Blood pressure of rats fed the diet with cadmium decreased after 8 wk, but this effect was counteracted by dietary nickel. Cadmium caused a depletion of iron and resulted in an accumulation of zinc in liver and kidney of rats. Nickel partially counteracted the iron loss due to cadmium. In a second experiment, the inclusion of 10 or 20 ppm cadmium in drinking water for 24 mo did not result in elevated blood pressure in normal or genetically hypertensive rats. Cadmium had no effect on the plasma renin levels in either experiment. Low intake of cadmium (10 or 20 ppm) in drinking water resulted in elevated cadmium content in hair. Thus, our data do not indicate that high levels of cadmium contribute to hypertension.
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PMID:Cadmium and nickel influence on blood pressure, plasma renin, and tissue mineral concentrations. 698 93

The permeability of the endothelium of the aorta in hypertensive rats with normal and high plasma renin activity was studied with colloidal iron. In the former it was normal while in the latter it was markedly increased. It is concluded that the increased permeability is due to the high renin and not to the elevated blood pressure.
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PMID:[Changes of the permeability of the aortic endothelium in renovascular hypertension in the rat (preliminary data)]. 738 90

In this study, disturbance of immune response as a pathogenic mechanism for human volume hypertension was investigated and compared to nephritis in its correlation with the metals such as zinc, iron and aluminum as environmental factors. Urinary gamma-GTP excretions in patients with nephritis or hypertension were higher than in healthy people, whereas the plasma renin activity in these patients were lower on the average than in healthy individuals. Hypertensive patients participating in this study were diagnosed as the volume hypertension type from our clinical and other results. The serum IgM and IgA levels in renal patients showed a tendency to be lower than in the healthy people used as control. Urinary IgA excretion in hypertensive patients was increased in association with increasing excretions of aluminum and/or iron into urine. The values of regression coefficients in the urine samples for aluminum and iron vs. IgA, respectively, were very high at r = 0.900 (n = 9, p < 0.05) and 0.736 (n = 9, p < 0.05). These correlations were shown to be very useful indicators in diagnosing volume hypertension. Moreover, hypertensive patients in this study were demonstrated to have a high regression coefficient (r = -0.702, n = 7; p < 0.05) for calcium vs. renin in the serum. In the hypertension, augmentation of serum calcium significantly decreased plasma renin activity.
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PMID:Changes in IgA and metals in serum and urine of human volume hypertension. 765 42

The purpose of recent studies was to investigate the expression of angiotensin II (Ang II) receptor sites in afferent arterioles freshly isolated from the rat kidney, and the role of Ang II on renin release by these vessels. The method of isolation and purification of renal microvessels was based on iron oxide infusion into the kidneys and separation of the afferent arterioles from glomeruli and connective tissue with the aid of a magnetic field, successive passages through various sieves, and harvesting with collagenase. Ang II receptor characteristics were evaluated by radioligand binding studies using the non-peptide Ang II antagonists of AT1 (Dup-753 and -532) and AT2 (PD-123319 and CGP-42112) receptors. AT1 antagonists displaced up to 80% of the Ang II binding with high affinity (3 nM), whereas the remaining 20% showed low affinity for the Dup compounds and CGP-42112 (> 10 microM), and intermediate affinity for PD-123319 (12 microM). These data suggest the existence of two Ang II receptor subtypes in the renal vasculature of the rat. In separate experiments, renin release by isolated afferent arterioles in vitro was 9 ng/hr/mg under control conditions. Ang II (0.1 microM) inhibited renin secretion by 20%, whereas the adenylyl cyclase activator forskolin (10 microM) stimulated renin secretion by 50%. In arterioles isolated from rats chronically treated with a converting enzyme inhibitor (perindoprilate) to reduce endogenous formation of Ang II, renin release increased 20-fold under control conditions in vitro and was further stimulated by forskolin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin II receptors and renin release in rat glomerular afferent arterioles. 770 9

We compared some of our latest experiments on blood pressure control and erythrocytosis in spontaneously hypertensive rats with Gaar's computer-simulated studies, which suggest that erythrocytosis is a key to understanding the hemodynamic changes in hypertension. We tested two of Gaar's several predictions: (i) peripheral vascular resistance decreases when the feedback control of erythrocytosis is blocked and (ii) in primary hypertension, blood volume is increased slightly. We also studied the interrelation of systolic blood pressure and plasma renin substrate in spontaneously hypertensive rats, and the effect of diet on renin, blood pressure, and erythrocytosis. Our data showed that (i) on a percentage basis the renin system supports blood pressure essentially in the same manner in normal and hypertensive rats, (ii) peripheral vascular resistance decreased when erythrocytosis was partially blocked by feeding a low-iron diet, (iii) blood volume was similar in normal and hypertensive rats, and (iv) dextrin stimulates plasma renin, packed cell volume, and blood pressure in hypertensive rats. We conclude that blood pressure and erythrocytosis are interrelated, that the combined data of stimulated and experimental studies support the notion that primary hypertension is a blood-vessel adaptation in response to a renal energy need that may require additional oxygen.
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PMID:Blood pressure control and erythrocytosis in rats: theory and observations. 795

The intracellular concentrations of calcium and chloride have been suggested to be involved in the control of renin secretion from juxtaglomerular (JG) cells. We have tested these propositions on permeabilized JG cells. Rat glomeruli with attached JG cells were isolated by the magnetic iron technique, superfused, and permeabilized by 20 microM digitonin for 12 min. The calcium concentration was varied with Ca ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) buffers [0 (5 MM EGTA without calcium), 17, 73, 170, 440, or 700 nM and 1.5, 15 or 150 microM]. These maneuvers had no effect on renin release, while 1.5 mM calcium caused a stimulation, which was not inhibited by 50 mM sucrose. Isosmotic increases in the chloride concentration to 25, 60, and 132 mM resulted in prompt stimulations of renin release. Similarly, iodide and nitrate stimulated renin release. We conclude that renin release from permeabilized JG cells is unaffected by calcium concentrations in the nano- and micromolar range, while the release is stimulated by chloride or other permeant anions. We suggest that in intact JG cells an increase in calcium inhibits renin release through activation of chloride channels followed by a drop in the intracellular chloride concentration. The stimulation caused by the high calcium concentration may be a toxic effect or may be due to stimulation of the fusion between granules and cell membrane in a way analogous to other secretory cells.
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PMID:Renin release from permeabilized juxtaglomerular cells is stimulated by chloride but not by low calcium. 818 93

Recent studies suggest the existence of a relationship between the renin-angiotensin system and erythropoietin (EPO) secretion. It has been studied whether patients with various forms of arterial hypertension (essential, renal, renovascular, in the course of arteritis) differ with respect to EPO secretion and whether EPO serum levels are related to renin response induced by dietary sodium restriction to 10-20 mmol Na/24 h for 3 days and upright body position for 3 h. Patients with different forms of hypertension and normal renal excretory function and healthy subjects did not differ in hematocrit value, markers of iron metabolism, and EPO secretion except for patients with arteritis who had higher ferritin values. In these patients a positive correlation between EPO levels and hematocrit values suggests the existence of an altered regulation of EPO secretion. In essential hypertension a negative correlation found between changes in EPO and PRA levels in response to sodium restriction and upright body position may also reflect an altered regulation of both EPO and renin production.
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PMID:Influence of the renin-angiotensin system stimulation on erythropoietin production in patients with various forms of arterial hypertension. 830 4

Over the 20-year period since the first issue of Environmental Health Perspectives was published, there has been considerable progress in the understanding of the potential toxicity of exposure to lead. Many of these advances have been reviewed in published symposia, conferences, and review papers in EHP. This brief review identifies major advances as well as a number of current concerns that present opportunities for prevention and intervention strategies. The major scientific advance has been the demonstration that blood lead (PbB) levels of 10-15 micrograms/dL in newborn and very young infants result in cognitive and behavioral deficits. Further support for this observation is being obtained by prospective or longitudinal studies presently in progress. The mechanism(s) for the central nervous system effects of lead is unclear but involve lead interactions within calcium-mediated intracellular messenger systems and neurotransmission. Effects of low-level lead exposure on blood pressure, particularly in adult men, may be related to the effect of lead on calcium-mediated control of vascular smooth muscle contraction and on the renin-angiotensin system. Reproductive effects of lead have long been suspected, but low-level effects have not been well studied. Whether lead is a carcinogen or its association with renal adenocarcinoma is a consequence of cystic nephropathy is uncertain. Major risk factors for lead toxicity in children in the United States include nutrition, particularly deficiencies of essential metals, calcium, iron, and zinc, and housing and socioeconomic status. A goal for the year 2000 is to reduce prevalence of blood lead levels exceeding 15 micrograms/dL.
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PMID:Lead toxicity: current concerns. 835 66


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