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)

The subcellular distribution and nature of rat renal renin has been investigated by means of analytical subcellular fractionation and gel filtration on Sephadex G-100. During differential centrifugation, renin activity was recovered mainly in soluble and heavy mitochondrial fractions. On sucrose gradient centrifugation in either a conventional or in a B XIV zonal rotor, renin activity equilibrated at 1.54 M sucrose and was partially resolved from marker enzymes for mitochondria (succinate dehydrogenase), lysosomes (acid phosphatase), plasma membranes (alkaline phosphatase), and peroxisomes (catalase). On gel filtration of the soluble or extracts of the renin-granular fractions on Sephadex G-100, renin activity eluted as a single peak with an apparent molecular weight (MW) of 42,000; no change in activity was found when these fractions were acidified to pH 3.0. When kidney homogenates were prepared in the presence of the proteolytic inhibitor N-ethylmaleimide (NEM, 10 mM), whereas the renin from the granular fractions displayed a MW of 44,000, that from the soluble fraction was apparently higher (69,000). Addition of NEM (10 mM) to the soluble fraction previously shown to contain only the low MW form of renin also resulted in an apparently high MW form of renin. These results indicate that rat renal renin is associated with a mechanically fragile, distinct type of subcellular organelle. Renin within this structure is of the low MW form and is not acid activatable. The soluble fraction, however, contains a factor(s) that, in the presence of NEM, combines with the low MW renin to form a complex of apparently high MW.
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PMID:Subcellular distribution and storage form of rat renal renin. 699 67

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in hemodialyzed patients. Two groups of hemodialyzed patients, each of which comprised 17 subjects, were examined. The first group was treated by EPO (EPO group) while the second one did not receive this hormone (No-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9, and 12 month points of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex- and age-matched healthy subjects. After EPO therapy, an increase of the hematocrit value from 21.8 +/- 0.9 to 32.6 +/- 0.9% was observed, which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the No-EPO group, a significant although less marked rise of the hematocrit value (21.4 +/- 0.4 to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change plasma levels of electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose, and alkaline phosphatase as well as plasma concentrations of calcium-related hormones (PTH, calcitonin, 1,25[OH]2D3), vasopressin, and triiodothyronine. EPO treatment induced a significant decrease in somatotropin, prolactin, follitropin, lutropin, ACTH, cortisol, plasma renin activity, aldosterone, noradrenaline, adrenaline, dopamine, glucagon, pancreatic polypeptide, and gastrin plasma levels and an increase in plasma insulin, estradiol, testosterone, atrial natriuretic peptide, thyrotropin, and thyroxine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Function of endocrine organs in hemodialyzed patients of long-term erythropoietin therapy. 762 22

Immortalized rat proximal tubule cell (IRPTC) lines should be useful for investigation of proximal tubule (PT) regulation and function but previously have been unavailable. We now report the establishment and characterization of an immortalized transformed, temperature-sensitive IRPTC cell line containing renin-angiotensin system (RAS) components. Primary PT cells prepared from male Wistar rats (4-5 wk old) after collagenase digestion, sieving, and Percoll gradient were cultured on collagen-coated T-75 flasks in Dulbecco's modified Eagle's medium containing 5% fetal calf serum. Subconfluent PT cells were transfected with the temperature-sensitive SV40 mutant viruses (tsA SV40) by direct exposure. After 7-8 wk, several clones were obtained, from which one has been characterized and designated as line 3-2. This cell line appears stable up to 45 passages. Clonal cells transformed with this virus exhibit a transformed phenotype at a permissive temperature of 34 degrees C and grow in multiple layers. When the cells are subsequently placed at a nonpermissive temperature of 41 degrees C, they return to morphology similar to that of untransformed cells of the same lineage. At either 34 degrees C or 41 degrees C, this cell line expresses a variety of PT markers including alkaline phosphatase, cytokeratin, carbonic anhydrase, and glucose transporter isoform 2 (GLUT2), while not expressing factor VIII. Uniquely, these cells also appear to express PT proteins gp330 and CHIP28, markers which are usually lost in cultured cells. Furthermore, the cell line expresses protein and mRNA components of RAS, including angiotensinogen, angiotensin converting enzyme, and renin. The IRPTC cell line expresses few angiotensin II (ANG II) receptors at 34 degrees C, the permissive temperature. However, at the nonpermissive temperature, 41 degrees C, IRPTC expresses ANG II receptor (dissociation constant of 0.7 nM; maximum binding capacity of 265 fmol/mg protein). ANG II (10(-8) M) induced a transient rise in cytoplasmic Ca2+ concentration, which was nearly abolished with losartan but not PD-123319, suggesting this finding is AT1 receptor mediated. This cell line should provide an excellent model of PT and should make it possible to study the cell and molecular biology of the RAS, as well as other regulatory systems of the PT.
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PMID:Temperature-sensitive SV40 immortalized rat proximal tubule cell line has functional renin-angiotensin system. 790 Aug 43

Human decidual tissue consists of a heterogeneous population of cells, including stromal cells, lymphocytes, and macrophages. Lipopolysaccharides (LPS), which bind to specific cell surface receptors on macrophages, have been shown to increase prostaglandin production by the decidua and amnion. To determine whether LPS may also affect decidual hormone production, we have examined the effects of LPS on the synthesis and release of prolactin and renin. Dispersed cells from term decidual tissue exposed to LPS L2880 (Escherichia coli, 1 microgram/ml) released significantly less prolactin and renin than control cells after 24 h of exposure. Maximal inhibition of prolactin (31.6%) and renin (62.5%) release was noted at 72 and 96 h of exposure, respectively (p < or = 0.0002 in each instance). The inhibition of prolactin and renin release was dose-dependent, with half-maximal inhibition at a dose of approximately 10 ng/ml. LPS caused a decrease in prolactin synthesis as well as release. In addition, LPS inhibited the stimulation of prolactin release in response to insulin, a known secretagogue of prolactin release. After 24, 48, and 72 h of exposure, the magnitude of the stimulation of prolactin release by cells exposed to insulin (100 ng/ml) in the presence of LPS (1 microgram/ml) was 84.5, 57.5, and 35.2% less, respectively, than that of cells exposed to insulin alone (p = 0.0001 in each instance). LPS L6011 (Salmonella endotoxin) also inhibited prolactin and renin release. LPS had no effect on overall protein or DNA synthesis and did not cause release of alkaline phosphatase and lactate dehydrogenase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipopolysaccharides inhibit prolactin and renin release from human decidual cells. 831 45

Six cases of tubular disorder of antenatal onset responsible for biological manifestations characteristic of Bartter syndrome and severe hypercalciuria are reported. In all six cases, severe hydramnios occurred during pregnancy between the 26th and 28th week after the last menstrual period. All six patients were born prematurely; gestational age ranged from 20 to 35 weeks. Major polyuria with dehydration occurred immediately after birth. The amounts of water and sodium needed to compensate urinary losses ranged from 280 to 370 ml/kg/day and 25 to 43 mmol/kg/d, respectively, during the first two postnatal months. Decreased serum potassium levels and increased plasma levels of renin and aldosterone were seen in all six patients. Increased urinary excretion of calcium was evidenced during the first postnatal week in three cases. Urinary calcium excretion in the six patients ranged from 15 to 30 mg/kg/d. Nephrocalcinosis developed in all six patients and two patients developed urinary lithiasis. One patient died at one month of age from necrotizing enteropathy. The five remaining patients gradually developed severe growth failure with measurements between 4 and 5.5 SDs below the mean. These five patients had evidence of hyperparathyroidism including increased serum levels of parathyroid hormone (5/5), increased serum alkaline phosphatase activity (4/5), and roentgenographic bone changes (1/5). Ionized calcium assays performed in three of the five patients disclosed low values (range 1.25-1.47 mmol/l; mean = 1.35; normal values = 1.42-1.62), although total serum calcium levels were normal or high (range 2.16-2.98 mmol/l; mean 2.61; normal values = 2.45-2.65) probably as a result of chronic dehydration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antenatal form of Bartter's syndrome]. 845 38

The mechanisms and myocardial alterations associated with NO-deficient hypertension are still far from clear. The aim of the present study was to focus on the enzyme histochemical and subcellular changes in the heart of L-NAME treated rats, as well as to examine the influence of captopril treatment. Wistar rats were administered either L-NAME (40 mg/kg/day) alone or together with captopril (100 mg/kg/day) for a period of 4 weeks. A significant increase of blood pressure confirmed the reliability of the model. The results showed that long-lasting L-NAME administration was accompanied by a decrease of endothelial NO-synthase activity and by a significant local decrease of the following enzyme activities: capillary-related alkaline phosphatase, 5'-nucleotidase and ATPase (but not dipeptidyl peptidase IV) and cardiomyocyte-related glycogen phosphorylase, succinic dehydrogenase, beta-hydroxybutyrate dehydrogenase and ATPases. No activity of these enzymes was found in the scar, whereas a marked increase of alkaline phosphatase and dipeptidyl peptidase IV activities was found in the foci of fibrotization. Histochemical changes correlated with subcellular changes, which were characterized by 1) apparent fibroblast activation associated with interstitial/perivascular fibrosis, 2) heterogeneous population of the normal, hypertrophic and injured cardiomyocytes, 3) enhancement of the atrial granules and their translocation into the sarcolemma, and 4) impairment of capillaries as well as by induction of angiogenesis. Similar alterations were also found in the heart of captopril co-treated rats, despite of the significant suppression of blood pressure. The results indicate that NO-deficient hypertension is accompanied by metabolic disturbances and ultrastructural alterations of the heart and these changes are probably not induced by the renin-angiotension system only.
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PMID:Chronic disturbances in NO production results in histochemical and subcellular alterations of the rat heart. 1080 8

In a 10-year-old castrated male shorthaired German pointer polyuria was associated with slight hypokalemia, hypophosphatemia and alkalosis, as well as elevated plasma concentrations of a glucocorticoid-inducible iso-enzyme of alkaline phosphatase. Repeated measurements of urinary corticoids and normal suppressibility of the hypothalamus-pituitary-adrenocorticial axis excluded glucocorticoid excess. Urine osmolality (Uosm) did not increase during administration of the vasopressin analogue desmopressin. At the time water deprivation had caused Uosm to rise from 300 to 788 mOsm/kg, there was also plasma hypertonicity. During hypertonic saline infusion the osmotic threshold for vasopressin release was increased. The combination of elevated plasma aldosterone concentrations and unmeasurably low plasma renin activity pointed to primary hyperaldosteronism. As initially computed tomography (CT) did not reveal an adrenocortical lesion, the dog was treated with the aldosterone antagonist spironolactone. This caused Uosm to rise in a dose-dependent manner. However, well-concentrated urine was only achieved with doses that gave rise to adverse effects. Once repeated CT, using 2-mm-thick slices, had revealed a small nodule in the cranial pole of the left adrenal, unilateral adrenalectomy was performed which resolved the polyuria completely. Also the plasma concentrations of kalium, aldosterone and renin activity returned to within their respective reference ranges. The adrenocortical nodule had the histological characteristics of an aldosteronoma, with the non-affected zona glomerulosa being atrophic.In this dog with primary hyperaldosteronism the polyuria was characterized by vasopressin resistance and increased osmotic threshold of vasopressin release, similar to the polyuria of glucocorticoid excess. The possibility is discussed that the polyuria of glucocorticoid excess is actually a mineralocorticoid effect.
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PMID:Aldosteronoma in a dog with polyuria as the leading symptom. 1143 3

An intense activity of enzymes which actively participate in the renin-angiotensin-aldosterone system was shown in extravillous trophoblast cells which are involved in the performing of spiral arteries into uteroplacental vessels. The hydrolase activity in villous trophoblast underwent important variations, but it was constant in cells of the extravillous trophoblast. Activity of lysosomal hydrolases, of leucine aminopeptidase and N-acetyl glucosaminidase type, was markedly positive in X-cells, while negative in the villous trophoblast. Beta glucuronidase activity has shown moderate activity in cells of extravillous trophoblast, while in villous trophoblast it was weakly emphasized or negative. Intense activity of prostaglandin E2 dehydrogenase in the way of strongly emphasized microsomal reaction was noted exclusively in extravillous cells of basal plate, especially in perivascular cell groupings. Within all examined enzymes activities, only the membranous activity of alkaline phosphatase was of the same intensity in cells of extravillous trophoblast. Lacking of penetration of these cells into the spiral arteries wall in EPH-gestosis, which also means loss of their close contact with the blood of a pregnant, implicates the practical meaning of these observations.
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PMID:Histoenzymatic and immunocytochemical characteristics of extravillous trophoblast cells of placental basal plate as parameter of their function in hypertensive pregnancy. 1213 10

The possible hormonal interactions of parathormone and extracellular calcium level with other endocrine systems were studied. Primary hyperparathyroidism was used first as a clinical model, in which hypercalcemia and normocalcemia occurs before and after surgery, respectively. An increased activity of renin-aldosterone system related to parathormone was found in hyperparathyroidism, and surgery resulted in a small decrease in blood pressure. This change was accompanied by a significant decrease in the activity of the renin-aldosterone system indicating the cessation of the secondary hyperaldosteronism. The role of a relative hyperinsulinism, occurring in hyperparathyroidism, in the pathogenesis of hypertension was not proved. The basal and stimulated secretion of thyreotrophin, the basal growth hormone level, and the stimulated prolactin secretion increased after surgery. Follicle stimulating hormone and luteinizing hormone secretions remained unchanged. The results suggest that extracellular calcium may reversibly modify the secretion of certain anterior pituitary hormones and their stimulus-induced responses. In the second disease, growth hormone deficiency syndrome, studied, long-term growth hormone replacement therapy results in significant but transient changes in bone metabolism: calcium-, alkaline phosphatase-, and phosphate levels increase until 6 to 18 months as compared to the initial values; then these parameters decrease to the baseline level. Parathormone decreases until the first year then returns to the baseline level. Osteocalcin shows similar temporary changes. In spite of the above transient changes, osteodensity increases after 12 months of treatment, and further improvement can be seen after 18 and 24 months, i.e. GH treatment exerts a biphasic effect on bones; resorption increases first followed by an increase in formation. Based on the above results, it can be concluded that both parathormone and extracellular calcium are able to influence the secretion of certain hormones; and--as it is shown in growth hormone replacement therapy--other hormones may cause certain effect on them, too. The better understanding of these interactions may result in a better understanding of the pathomechanism of certain diseases and the improvement of their treatment.
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PMID:[Hormonal interactions of parathormone and calcium metabolism]. 1263 47

Bartter's syndrome is characterized by hypochloremia, hypokalemia, metabolic alkalosis associated with renal potassium leakage, and normal blood pressure despite increased plasma renin activity. Although association of empty sella with Gitelman syndrome has been reported, no association has been reported with Bartter's syndrome. Here we report a patient with Bartter's syndrome and empty sella. A 12 month-old male patient presented with a history of nausea, vomiting, abdominal distension, constipation, and edema in the lower extremities that had begun in the early postnatal period. The patient was born at 32 weeks gestation by operative delivery for polyhydramnios. Blood pressure was normal. Serum sodium, potassium, calcium, phosphate, chloride, albumin and alkaline phosphatase levels were 129 mEq/l, 2.5 mEq/l, 9 mg/dl, 3.8 mg/dl, 72 mg/dl, 4.2 g/dl and 1285 IU/l, respectively. Serum magnesium level was normal. Arterial blood gas levels revealed pH 7.55 (normal, 7.35-7.45), PCO2 33.6 mm/Hg (36-46), base excess +7.1 (+/- 2.3), and total CO2 33.6 mmol/l (23-27). Renin and aldosterone levels were elevated. Urine had pH 8.0 and specific gravity 1.010. Urinary calcium excretion was 22.8 kg/day (urine calcium/creatinine ratio 0.46). Urinary potassium and chloride levels were elevated. MRI of the brain was normal except for partially empty sella. We present the first pediatric patient with the association of Bartter's syndrome and empty sella.
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PMID:Association of Bartter's syndrome and empty sella. 1451 87


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