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

Dogs given excess vitamin D (500 or 1,000 micrograms/kg of body weight each day for 1 to 3 weeks were observed for clinical and pathologic changes of increased blood pressure and of characteristic nephropathy associated with vitamin D toxicosis or hypercalcemia. Serum calcium and serum urea nitrogen (UN) increased throughout the treatment period, but serum phosphorus remained within the normal range. Plasma renin activity increased markedly. Blood pressure showed only insignificnat changes (P = greater than 0.05). Gross and microscopic examination of the kidneys suggested vascular-oriented changes with an ischemic basis. Glomerular vascular poles showed hypertrophy and hyperplasia of juxtaglomerular cells. Ultrastructually, an increase in the number of secretory granules was noticed in these cells. A hypothesis regarding the mechanism of renal injury during vitamin D toxicosis is presented.
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PMID:Vitamin D intoxication and the pathogenesis of vitamin D nephropathy in the dog. 45 87

In conclusion, patients on chronic maintenance dialysis have an increased incidence of death from cardiovascular disease. Hypertension plays a major role, and these patients must be carefully monitored for complete control of blood pressure. Adequacy of ultrafiltration to maintain normal extracellular volume is an essential part of the dialytic treatment. Hypertensive patients should be screened for excessive renin secretion because of its possible role in unresponsive hypertension in patients on dialysis. Nephrectomy should be used when necessary, where dialysis and antihypertensive medication have not adequately controlled blood pressure. Patients must be monitored for the presence of pericardial disease to avoid subsequent pericardial effusion and the development of constrictive pericarditis with its adverse effect on myocardial function. When constrictive pericarditis is present, it obviously should be relieved by appropriate surgery. Efforts should be made to minimize cardiac output in hemodialysis patients. Whether or not routine transfusions to maintain a higher hematocrit are indicated is a question that cannot yet be answered. However, patients with marginal cardiovascular function who are accepted on hemodialysis and must have an arteriovenous shunt should be supported in any manner to minimize an increase in cardiac output. Early and aggressive treatment of known episodes of sepsis is important in the elimination of valvular endocarditis in this patient population. Perhaps one of the finer indicators of adequacy of hemodialysis will be K rate and peak immunoreactive insulin levels. Continued abnormality of these parameters may contribute to cardiovascular disease. Clearly, further study of the effect of abnormal carbohydrate metabolism on lipid metabolism is in order. Serum triglyceride, serum cholesterol and lipid electrophoretic pattern should be followed to evaluate the beneficial effects of drug therapy and changes in dialytic technique on the development of cardiovascular disease. Careful monitoring of calcium, phosphorus, bone films and parathyroid hormone levels is indicated to assess parathyroid status. The use of aluminum binders and parathyroidectomy to prevent vascular and myocardial calcification is important in the therapy of these patients. The use of cardiac catheterization, coronary artery arteriography, and possibly cardiac vascular repair, should be considered in the chronic hemodialysis patient with coronary artery disease if he is otherwise well. Adequacy of hemodialysis perhaps can be evaluated through its effect on all of the above parameters. Whether or not changes in artificial kidney treatments can correct the final vascular disease remains to be seen.
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PMID:Cardiovascular disease in uremic patients on hemodialysis. 109 1

Eight normotensive white middle-aged men were given low, moderate, and high salt diets with constant potassium intakes each for periods of at least 4 weeks. There was a tendency for body weight, serum sodium, exchangeable sodium, and inulin space to increase. Indirect blood pressure measurements revealed no change in blood pressure, either supine or upright measurements, during the 3 study intervals. Inulin clearance (and presumably glomerular filtration rate) rose with increase in dietary salt. Urinary potassium excretion rose progressively as salt intake increased. Total body potassium tended to decrease with increase in dietary salt. There was no changes in the excretion of calcium, magnesium, phosphorus, nor were there changes in the blood level of potassium. There was no change in total body water. The serum cholesterol and triglyceride levels were not appreciably affected by the different dietary sodium intakes. Plasma renin activity and urinary aldosterone excretion rose progressively with the two levels of sodium restriction. These studies indicate that normal man is able to compensate for large differences in sodium intake with minor metabolic changes. These changes do not necessarily lead to hypertension over a one-month period. Nevertheless, many hemodynamic and hormonal compensatory mechanisms come into play. It is evident that hypertension might result should the sodium load not be excreted, the circulating volume become too great for the excretory capacity, or if neural or endocrine adjustments be inadequate.
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PMID:The effect of dietary sodium chloride on blood pressure, body fluids, electrolytes, renal function, and serum lipids of normotensive man. 124 73

The renal effect of cyclic somatostatin was studied on healthy subjects. The somatostatin was used at therapeutical dose in intravenous infusion. Somatostatin decreases the renal plasma flow, glomerular filtration rate, osmotic and free water clearances, sodium and potassium excretion and the tubular reabsorption of phosphorus while urinary osmolality increases. Under somatostatin infusion the urinary excretion of catecholamines, PGE2, PGF2 alfa and the plasma renin activity and the plasma concentration of glucagon and growth hormone decrease. The antidiuretic activity of somatostatin is due to a) a direct haemodinamic effect, b) an influence on the renal tubular transport as well and also c) because of change the water handling in the collecting ducts.
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PMID:[Effect of somatostatin on kidney function]. 168 89

Recombinant interleukin-2 (rIL-2) is a new promising treatment for cancer, but is associated with severe renal toxicity. This study is the first to analyse the renal effects of rIL-2 in children. Twenty-one cycles of continuous rIL-2 infusion were studied in 15 patients; mean age was 6.9 years and average weight 18.9 kg. Interstitial fluid retention and oliguria (baseline, 1.7 ml/kg per hour; nadir, 0.5 mg/kg per hour) were associated with hypotension (baseline, 101/56 mm Hg; nadir, 85/43 mm Hg) and decreased intravascular volume (plasma renin activity increased x 10). Weight gain (+7.9%) was observed in 13 cycles whereas weight loss (-6.3%) was shown in 8 cycles because of digestive and cutaneous losses, mainly in the youngest patients. This prerenal azotaemia was characterized by a decrease in creatinine clearance (from 101 to 36 ml/min per 1.73 m2) and a low fractional excretion of sodium (FENa) (from 0.70% to 0.09%). Hypotension and hypovolaemia needed vascular filling (n = 12), dopamine (n = 7) and interruption of rIL-2 (n = 2). Most abnormalities occurred as early as day 2 of therapy and were always reversible after a short period with sodium leakage (diuresis = 2.2 ml/kg per hour, FENa = 2.01%). Hypophosphataemia was associated with low urinary excretion of phosphorus, suggesting an increased uptake of inorganic phosphorus by rapidly proliferating lymphoid cells.
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PMID:Renal effects of continuous infusion of recombinant interleukin-2 in children. 202 34

Several abnormalities of calcium metabolism have been described in patients with essential hypertension, and they have been linked to the pathogenesis of hypertension. Intestinal calcium absorption has been shown to be decreased in rats with spontaneous hypertension, but it has not been studied in patients with essential hypertension. In these studies we have for the first time measured intestinal absorption of calcium (using oral and intravenous administration of 47Ca), along with other parameters of calcium metabolism, in 14 patients with essential hypertension and normal renal function and in 16 normal subjects. There was no difference in serum total or ionized calcium, serum phosphorus, parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D), and 24,25-dihydroxy-vitamin D(24,25(OH)2D) among hypertensives and normotensives. The urinary excretion of calcium, on the other hand, was greater in hypertensive than in normotensive subjects (195 +/- 33 v 107 +/- 13 mg/24 h, P less than .05). There was also no difference in intestinal absorption of calcium after 2 and 24 h among hypertensives and normotensives. When hypertensive patients were stratified according to plasma renin activity (PRA) we found that patients with low PRA had higher intestinal absorption of calcium at 2 h (23 +/- 2.9 v 18 +/- 0.6%, P less than .05) but not at 24 h. Serum total and ionized calcium, PTH, and 1,25(OH)2D were not different between patients with low and those with normal-high PRA. The major derangement of calcium metabolism in patients with essential hypertension is hypercalciuria. This abnormality is more pronounced in patients with low PRA, and it may lead to increased vitamin D-dependent intestinal absorption of calcium.
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PMID:Intestinal absorption of calcium and calcium metabolism in patients with essential hypertension and normal renal function. 206 73

The effects of an orally active inhibitor (UK 79300) of the neutral metalloendopeptidase EC 3.4.24.11 were investigated in six healthy male volunteers maintained on a constant diet (150 mmol sodium/day and 80 mmol potassium/day). Subjects were studied in a random order, single-blind study on two occasions, each 48 hours in length, when they were given UK 79300 (25 or 50 mg p.o.) or placebo at 12-hour intervals (each agent for 24 hours). The endopeptidase inhibitor enhanced plasma concentrations of atrial natriuretic factor in association with suppression of both plasma renin activity and aldosterone concentrations. Twenty-four-hour urinary excretion of sodium was doubled by UK 79300, and the urinary excretion rates of phosphorus, atrial natriuretic factor immunoreactivity, and cyclic guanosine monophosphate were also significantly enhanced, whereas urinary aldosterone excretion was halved. The profile of biological effects closely paralleled those previously reported with low dose infusions of atrial natriuretic factor in humans and animals. Therapeutic trials of such inhibitors are now indicated for hypertension or heart failure together with further studies to clarify the underlying mechanisms of action.
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PMID:Inhibition of endopeptidase EC 24.11 in humans. Renal and endocrine effects. 214 60

We evaluated the effect of a low potassium diet on blood pressure in normotensive (NT) and in borderline hypertensive subjects (BHT). There were 11 BHT men (age, 24.6 +/- 1.2 years) and 10 NT men (age, 23.5 +/- 1.0 years). Subjects were studied while on both low potassium, high sodium (30 meq/day, 400 meq/day) diets and high potassium, high sodium (100 meq/day, 400 meq/day) diets, each taken for 6 days. During the low potassium diet, daytime ambulatory systolic blood pressure increased in both NT (123 +/- 5 mm Hg, low potassium, vs. 116 +/- 4 mm Hg, high potassium, p less than 0.01) and BHT groups (134 +/- 3, low potassium, vs. 124 +/- 3, high potassium, p less than 0.001). Mean blood pressure was not different in NT during the two diets but was significantly higher during the low potassium diet in BHT subjects (97 +/- 2 mm Hg low potassium, vs. 92 +/- 1 mm Hg, high potassium, p less than 0.05) without change in heart rate in BHT subjects during the two diets. Low potassium diet increased the postural rise in diastolic blood pressure when subjects changed from the supine position to quiet standing (standing diastolic blood pressure for NT: low potassium, 79 +/- 2 mm Hg vs. high potassium, 72 +/- 2 mm Hg; for BHT: low potassium, 89 +/- 2 mm Hg vs. high potassium diet, 83 +/- 2 mm Hg, p less than 0.01). The effects of low potassium diet on blood pressure were not related to marked changes in renal hemodynamics, in plasma renin activity, in aldosterone, or in norepinephrine, nor to increases in forearm vascular resistance or in muscle sympathetic nerve activity. In fact, muscle sympathetic nerve activity decreased in the BHT group during low potassium compared with high potassium diets (p less than 0.001) and did not change in the NT group. Sympathetic nerve activity was also higher in BHT compared with the NT group during high potassium and low potassium diets, p less than 0.001. In the NT group, the low potassium diet was associated with lower hematocrit levels, weight gain, and increased 24 hour urinary calcium levels. After the low potassium diet, serum potassium fell in both groups, and serum phosphorus fell significantly in the BHT group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of dietary potassium on blood pressure, renal function, muscle sympathetic nerve activity, and forearm vascular resistance and flow in normotensive and borderline hypertensive humans. 229 25

In studying the metabolic effects of diet potassium (K+) variation in normal humans, we noted that varying diet K+ within its normal range influenced inorganic phosphorus (Pi) homeostasis and serum calcitriol (1,25-dihydroxyvitamin D) levels. In six men who ingested a constant whole-foods diet containing (per 70 kg body wt) 27 mmol/day Pi and 52 mEq/day K+, we increased diet K+ to 156 mmol/day with supplements first of potassium bicarbonate (KHCO3) alone and then of potassium chloride (KCL) alone, each for eight days interrupted by an eight-day recovery period of no K+ supplement. Urine Pi decreased promptly with either K(+)-salt, each inducing a persisting retention of 7 to 10 mmoles Pi, which was dumped during recovery. Fasting serum [Pi] increased with either K+ supplement (P = 0.022, repeated measures analysis of variance); the composite mean serum [Pi] for the two K(+)-supplement periods exceeded that for the two periods without supplements (P less than 0.01, paired t-test). Conversely, the concentrations of serum calcitriol decreased with either K+ supplement (P = 0.020). Among subjects, the diet K(+)-induced increases in serum [Pi] correlated with those in plasma [K+] (r = 0.64, P = 0.027); the decreases in serum calcitriol concentration correlated with the increases in serum [Pi] (r = -0.69, P = 0.014). There were no significant differences among periods in serum parathyroid hormone, ionized calcium, urine cyclic AMP excretion, plasma renin activity, body weight, serum albumin, or creatinine clearance; plasma volume decreased slightly during KCL but not during KHCO3 periods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary potassium influences kidney maintenance of serum phosphorus concentration. 234 30


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