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)

Literature on the biochemical effects of oral contraceptives (OCs) is reviewed. The effects of OCs on concentrations of mineral elements ( calcium, phosphorus, magnesium, iron, copper, and zinc), vitamins (ascor bic acid, folic acid, and Vitamins-B6, B12, and E), hormones, (gonadotro pins, progesterone, estrogens, androgens, corticosteroids, aldosterone, renin-angiotensin, insulin, growth hormone, thyroid hormones, catecholamines, and prolactin), amino acids and proteins (free amino acids, tryptophan, metalloproteins, hormone-binding proteins, miscellaneous serum proteins, and blood coagulation factors), carbohydra tes (glucose tolerance tests, glucose metablism and other carbohydrates) , lipids (total serum lipids, triglycerides, phospholipids, fatty acids, and cholesterol), and enzymes (aminotransfereases, alkaline phosphatase, and glutamyltransferase) are reviewed. Changes induced by combined, sequential, and low-dose OCs in 116 biochemical parameters are summarized in a table.
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PMID:Biochemical effects of oral contraceptives. 18 Jul 84

Plasma renin activity (PRA) was measured in 14 control subjects and 27 patients with essential hypertension (EH) (low renin group: 9, normal renin group: 11, and high renin group: 7) before and after the following stimulation tests. Test procedures: 1) Circadian rhythm (0600, 1600 and 2400h). 2) Adrenal stimulation test (ACTH: 12.5 I.U.). 3) Adrenal suppression test (Dexamethasone: 1.0 mg). 4) Metopirone test (1.5 g). 5) Angiotensin II infusion test (8 ng/kg/min). 6) Saline infusion test (1000 ml/hr). Patients with low PRA showed significantly lower levels of PRA than those of other two groups in circadian rhythm, after 2 hours of ACTH infusion and after angiotensin II infusion. Furthermore, these patients showed significantly higher responses of PRA than other two groups after furosemide test under dexamethasone and after metopirone test. In case of saline infusion test, patients with low and normal PRA did not show significantly decreased levels of PRA after the infusion, though all patients with high PRA and all control subjects showed significantly decreased levels of PRA. From the present studies, it might be concluded that patients with low PRA has an unknown mineralocorticoid excess which is ACTH dependent and 11 hydroxylated and some of hypertensive patients have an abnormality in their renin-angiotensin-aldosterone volume feed back loop as a factor for hypertension.
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PMID:Pathogenesis of essential hypertension with low renin: responses of plasma renin activity to various stimulation tests in essential hypertension. 21 18

Plasma volume is usually lower in patients with essential hypertension than in normal subjects. Normal or expanded plasma volume in some hypertensive patients may respect either a specific hypervolemic subset of the disease or the upper end of a continuum of volume values. Difficulties in defining these groups stem from the small numbers of subjects studied, from the need for a reliable reference index for volume measurements, and from the multiple factors which may affect intravascular volume. Differences in plasma volume cap influence choice of antihypertensive therapy; patients with expanded volume tend also to have slightly exchangeable sodium and greater extracellular fluid (ECF) volume and to respond well to diuretic therapy. There is also some evidence that low plasma renin activity is more frequent among hypervolemic patients. Essential hypertensives as a group have low plasma to interstitial fluid volume ratio (PV/IF), indicating that ECF distribution between the intravascular and interstitial compartments is shifted toward the latter. This is probably related to altered capillary filtration pressure due to increased venous resistance. Hypovolemic essential hypertensives have significantly lower (P less than 0.01) PV/IF ratio than hypervolemic, but whether this is related to differences in neural venous tone is only speculative. Hemodynamic studies revealed no difference in cardiac output between hypertensive patients with contracted blood volume and those with hypervolemia; total peripheral resistance was even higher in the latter, suggesting that "vasoconstriction" is not different between the two groups. It is widely believed that the relationship between ECF expansion and hypertension depends on the development of hypervolemia, increased cardiac output, and subsequent rise in total peripheral resistance reducing volume expansion and normalizing systemic flow while maintaining a high blood pressure. This sequence of events has been demonstrated in some human and experimental forms of hypertension but not in all. Metyrapone-induced hypertension in dogs could be sustained for up to 6 weeks by increased output with no evidence of "autoregulation" developing, and similar observations were reported in some anephric patients. Complementing these findings are observations of elevated cardiac output in some patients with long-standing essential hypertension or primary aldosteronism. It is therefore suggested that the spectrum of hemodynamic changes associated with volume disturbances in hypertension is too wide to be forced under one hypothesis alone and that neurogenic and other factors may play an important role in that complex relationship.
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PMID:Hemodynamic role of extracellular fluid in hypertension. 77 71

When rats are subjected to hypoxia, an increase in serum angiotensinogen concentration occurs which is accompanied by the appearance of serum erythropoietin (EP) during the first 24 h. Subsequent increases in EP reach maximum values 24 to 48 h after increases in packed cell volume (PCV) and serum renin levels. The current experiments were designed to determine if a decrease in iron stores is the stimulus for renin production when rats are rapidly expanding their red cell volume in a hypoxic environment. Young rats fed McCall's low iron diet were paired with rats fed the same diet supplemented with ferric citrate (6 g/kg diet). After two weeks at ambient pressure, they were subjected to hypoxia (0.48 atm) for 1 to 10 days. After 5 days at the reduced pressure, a fraction of the rats on the low iron diet were fed the iron-supplemented diet. At the time of sacrifice, serum was assayed for total iron binding capacity (TIBC) and renin. Rats that were fed the low iron diet showed an increase in TIBC, an increase in serum renin and a positive correlation between serum renin and TIBC. Rats that were fed a normal iron diet under the same conditions had lower TIBC, lower serum renin and no correlation between serum renin and TIBC. When low iron diet rats were supplemented with iron, TIBC and serum renin decreased. These experiments may have a clinical counterpart. The total iron binding capacity, renin and angiotensinogen were measured in the serum of women during the first 19 weeks of pregnancy. Women during early pregnancy showed an increase in TIBC, an increase of renin and angiotensinogen in the serum and a positive correlation between TIBC and renin concentration. It is suggested that the increased concentration of renin in the serum of women during the first 19 weeks of pregnancy and in the serum of rats that are rapidly expanding their red cell volume are related to a decrease in iron stores.
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PMID:The interrelation of renin and iron binding capacity. 97 91

1. A method is described for studying renin release from superfused rat glomeruli following their rapid isolation by a magnetic iron-oxide technique. 2. Microscopically selected glomeruli were free of tubular components. Some possessed vascular pole protrusions of up to 20 mum, unrelated to renin content. 3. Renin content of 102 batches, each of 400 glomeruli, was 1.34 plus or minus 0.08 times 10-4 Goldblatt hog units per 100 glomeruli (plus or minus S.E. of mean). Different osmolarities (305, 355 and 400 m-osmole/1.), sodium concentrations (110 and 135 mM) and buffer compositions of the preparation solution did not alter this value. Renin content per glomerulus in intact kidney was 100-fold higher. 4. At 30 degrees C the contained juxtaglomerular cells released renin at consistent but decreasing rates over 4-6 hr. Initial release rate in 110 mM sodium, 305 m-osmole/1. solutions were 0.86 plus or minus 0.068 times 10-6 units per 100 glomeruli per 30 min (plus or minus S.E. of mean, n = 42) or 0.546 plus or minus 0.046 percent of content per 30 min. In 135 mM sodium, 305 m-osmole/1. solutions, release was 2.4-fold higher (P less than 0.001) and remained elevated for at least 3 hr. When related to renin content per glomerulus resting release rate in vitro was higher by at most one order of magnitude than calculated in vivo values. 5. Release was augmented by gentle physical agitation of the glomeruli. 6. Release rate was inversely ralated to temperature. On reducing temperature from 30 degrees C, release increased 2.6-fold at 20 degrees C and 6.7-fold at 10 degrees C (P less than 0.001, n = 11). The response was reversible. 7. 3 mM sodium cyanide plus 3 mM sodium iodoacetate caused a variable release of renin associated with depletion of content within 4 hr. The response was progressive and reached a peak after 60 min. 8. Sensitivity of renin release to temperature and metabolic blockade indicates that energy is required for retention of renin by the cell. This, together with the release observed with increased sodium concentration at constant osmolarity, suggests a dependence of renin release upon the mechanism controlling the volume of the juxtaglomerular cell or its organelles.
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PMID:Characteristics of renin release from isolated superfused glomeruli in vitro. 113 91

Renal erythropoietin production is dependent on local oxygen content of blood which activates so called "oxygen sensors". Taking into consideration altered local renal blood supply in patients with arterial hypertension in the course of arteritis (HA) and from the other side contribution of the renin-angiotensin system in both pathogenesis of hypertension and regulation of erythropoietin production it seemed plausible to undertake this study. The aim of the study was to determine whether and in what extent patients with HA and healthy subjects differ in EPO secretion and whether EPO serum level is related in this patients to renin response to dietary sodium restriction and upright position of the body. 18 patients with HA and 12 healthy subjects were investigated. In all subjects haematocrit value, haemoglobin concentration, erythrocyte count, sodium, potassium, creatinine, iron, ferritin serum levels, total iron binding capacity, plasma renin activity (PRA), erythropoietin serum level and mean arterial blood pressure (MAP) were measured in basic conditions (normal sodium diet). Additionally PRA, EPO and MAP were measured after dietary sodium restriction to 10-20 mmol Na/24 hrs for three days and upright position of the body for three hours. Patients with HA had insignificantly lower serum EPO concentrations than healthy subjects and both studied groups did not differ in haematocrit value and determinants of iron metabolism except of significantly higher ferritin concentration in HA. After dietary sodium restriction and upright position of the body significant rise in PRA and no significant changes in EPO level were found in studied groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The role of erythropoietin in blood pressure regulation in patients with arteritis]. 130 May 62

To investigate whether newborn kidney microvessels and isolated single microvascular cells have the capacity to release renin and/or alter the expression of the renin gene in response to adenylate cyclase stimulation, newborn kidney microvessels were isolated and purified (95%) using an iron perfusion/enzymatic digestion technique. Incubation of microvessels with either vehicle (control; C) or 10(-5) M forskolin (F) in media resulted in an increase in microvessel cAMP (0.67 +/- 0.13 vs. 22 +/- 4.6 pmol/min per mg protein) (P less than 0.005) and renin released into the culture media (1,026 +/- 98 vs. 1,552 +/- 159 pg angiotensin I/h per mg protein) (P = 0.008) (C vs. F). Renin mRNA levels in the newborn kidney microvessels increased 1.6-fold with forskolin treatment. Renin release by isolated, single microvascular cells (with or without forskolin) was assessed using the reverse hemolytic plaque assay. Forskolin administration resulted in an increase in the number of renin-secreting cells without changes in the amount of renin secreted by individual cells. In conclusion, newborn kidney microvessels and isolated renin-releasing microvascular cells possess a functionally active adenylate cyclase whose short-term stimulation results in accumulation of cAMP, a significant increase in renin release, and an enhancement of renin gene expression. The increase in renin release is due to recruitment of microvascular cells secreting renin. Recruitment of hormone-secreting cells in response to stimuli may prove to be a mechanism of general biological importance shared by many endocrine cell types.
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PMID:Renin release and gene expression in intact rat kidney microvessels and single cells. 216 41

Preeclampsia is a complication of pregnancy characterized by hypertension, edema and proteinuria, beginning after 20 weeks of gestation. Six percent of the pregnant women in North America develop this disease, which is associated with increased morbidity and mortality for the mother and her baby. The physiopathology remains uncertain despite many research efforts. Actual hypotheses seek to explain the vasospasm that characterizes the disease. Among the many factors influencing vascular reactivity and possibly implicated are: the renin-angiotensin system, prostaglandins, progesterone and its metabolites, calcium, magnesium, digoxin-like immunoreactive substance(s), auricular natriuretic factor, substances secreted by platelets and leukotrienes. Prevention of the disease is limited by the absence of a biological or clinical marker with good sensitivity and appropriate specificity. Many biochemical or hematological parameters have been reported: uric acid, calcium, magnesium, proteinuria, blood iron, hematocrit, platelet count, antithrombin III, estrogen and progesterone. The combination of several tests could be superior to the use of each test individually, providing a better sensitivity and improving the positive predictive value. With early detection, new therapies for the prevention of the disease could be experimented on the higher risk women before the apparition of clinical symptoms or signs. Furthermore, those tests could be used in the study of the pathophysiology and in the choice of the best therapy.
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PMID:[Preeclampsia: physiopathology and prospects for early detection]. 269 75

Total and active renin were measured in plasma of 6 normal volunteers before and after acute and sustained angiotensin converting enzyme (ACE) inhibition with CGS 14824A (2 mg and 10 mg p.o. q.d.) or placebo treatment. The same sandwich technique was used for the measurement of both total and active renin using a polyacrylamide-iron-oxide linked monoclonal antibody to trap renin and 125I-labelled second monoclonal antirenin antibodies without or with specificity for active renin. Normal values for supine subjects ranged for active renin between less than 3 pg/ml and 28 pg/ml and for total renin between 73 and 263 pg/ml. Plasma ACE activity was clearly suppressed during 24 hours following both 2 mg and 10 mg CGS 14824A. Active plasma renin reached 6- and 12-fold normal values on days 1 and 7 of treatment with the 10 mg dose. Total renin rose to 150% and 228% respectively at the same time. Inactive renin continued rising during the first day of 10 mg CGS treatment to a final 141% at 24 hours post-drug and didn't change on day 7. Plasma renin activity correlated well with active renin levels (r = 0.92). We conclude that both total and active plasma renin concentrations can now be directly measured with great accuracy within 6 hours.
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PMID:Rapid measurement of total and active renin: plasma concentrations during acute and sustained converting enzyme inhibition with CGS 14824A. 282 Jun 26

The study was aimed to show whether the renin-angiotensin system acts on erythropoiesis in chronic renal failure patients with hemodialysis, since captopril leads to the worsening of anemia in such patients. The average dose of captopril in 13 cases studied was 19.3 mg per day and duration of the administration was 48 days. Blood-pressure fall by captopril was accompanied with the worsening of anemia. There were significant decreases in hemoglobin (8.3%), hematocrit (7.3%), red blood cell count (7.6%) and reticulocyte count (43.7%). Angiotensin II was significantly decreased (15.7%) with significant reductions of plasma aldosterone concentration (15.2%) and angiotensin-I converting enzyme (45.7%), and with significant increases in plasma renin activity (158.6%) and in angiotensin I (238.3%). However, plasma erythropoietin concentration remained unchanged. Serum iron concentration was slightly but significantly increased after captopril. Reticulocyte count was significantly correlated with AII either before (r = 0.716, p less than 0.01) or after captopril (r = 0.658, p less than 0.05). There was significant correlation between angiotensin II and red blood cell count before captopril (r = 0.710, p less than 0.01). It is concluded from the present study that the reduction of angiotensin II by captopril might contribute to the worsening of anemia seen in chronic hemodialysis patients.
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PMID:Participation of the renin-angiotensin system in the captopril-induced worsening of anemia in chronic hemodialysis patients. 352 28


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