Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:021525 (albumin)
 60,984 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were performed to evaluate the effects of the chronic administration of furosemide on hydrogen and electrolyte excretion in dogs on a normal electrolyte diet and in the absence of electrolyte or volume depletion. Control daily excretion in five dogs averaged 64 meq for Na, 51 meq for K, 66 meq for Cl, and 17 meq for net H. Furosemide, 40 mg, in the drinking water 3 times daily was given for 4 days. On day 1 Na excretion averaged 128 meq, but thereafter was not significantly different from control levels. Over 4 days cumulative net H excretion increased 63.6 meq and plasma HCO3 rose 6.6 meq/liter. The same dogs were restudied by the same protocol except that, to obviate electrolyte depletion, NaCl and KCl were administered daily in quantities sufficient to replace urinary losses. All dogs remained in positive Na, K, and Cl balance. Body weight, hematocrit, plasma albumin, creatinine, and plasma renin activity were unchanged, indicating the absence of electrolyte or volume depletion. Nonetheless, cumulative net H excretion increased 61.2 meq and plasma HCO3 increased 4.3 meq/liter. Two adrenalectomized dogs receiving steroid replacement showed similar changes in net H excretion and plasma HCO3. These experiments suggest that chronic furosemide administration may enhance H excretion and generate alkalosis even in the absence of volume or electrolyte depletion and without increased aldosterone secretion.
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PMID:Effect of chronic furosemide administration on hydrogen and sodium excretion in the dog. 1 99

Plasma concentrations of various physiologically important proteins, including transferrin, ceruloplasmin, haptoglobin, transcortin, sex hormone-binding globulin, thyroxin-binding globulin, renin-substrate, fibrinogen, coagulation factors VII and VIII, antithrombin-III, plasminogen, prealbumin, albumin, retinol-binding protein, and lipoprotein fractions, were measured before treatment with oral contraceptives (OCs) and then again after 6 cycles of treatment to measure changes in the daily synthesis rate of 2 proteins, albumin and fibrinogen, under the influence of various OC formulations. Results are presented for 38 women using high-dose (50 mcg estrogen) preparations, 38 using low-dose (30 mcg estrogen preparations), and 20 using a continuous-dose progestagen-only minipill (30 mcg levonorgestrel). Most of the proteins measured showed significant alterations in women using the high-dose OCs. Changes with the lower dose product were less marked, and most proteins were unchanged in women using the minipill. (For example, synthesis rates of fibrinogen, mg/kg/day, for controls, high-, low-, and mini-dose subjects were: 24, 43, 28, and 25 respectively). Data from isotope studies indicated that synthetic estrogens act on liver synthesis and secretion rates for many plasma proteins; hence the clinical associations seen with OC use.
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PMID:Oral contraceptives and plasma protein metabolism. 22 92

1. Two high-molecular-weight forms of renin (molecular weights 800 000 and 70 000) are present in mouse plasma. 2. The 800 000 form could be activated and converted into the fully active 40 000 form, by acid or limited proteolysis. The 70 000 form was activated without change in molecular weight. 3. In addition to its enzymic activity, renin was measured by a direct radioimmunoassay, which revealed that the current acid treatment of plasma did not activate all the renin present. 4. Renin is stored as fully active 40 000 renin, with a specific enzymic reactivity of 0.4 times 10(-3) GU ng(-1), in the submaxillary gland of mice. 5. Pure 125I-labelled 40 000 submaxillary renin did not bind to plasma proteins. However, by changing the tertiary structure of renin, it was bound to some of the plasma protease inhibitors; alpha2-macroglobulin, inter-alpha-trypsin inhibitor and alpha2-antithrombin. It was also bound to alpha1- and beta1-lipoprotein, albumin and an unidentified plasma protein. No binding was seen to more than 50 other studied plasma proteins.
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PMID:Is high-molecular-weight-renin binding of renin to the protease inhibitors and lipoproteins? 28 39

Five litter-mate male pigs, aged 7 days and fed a standard Pig Industry Board diet containing 190 g/kg dry mass of digestible protein, were compared with 10 male pigs from two litters fed a protein-deficient diet (50 g/kg) for a period of 70 days. The 10 experimental animals developed oedema between the 42nd and 70th days of the study and 4 of them became lethargic. Although the 10 experimental animals showed the typical biochemical changes characteristic of protein energy malnutrition (PEM), including changes in muscle electrolytes, liver fat and plasma albumin, the 4 lethargic animals showed a significant increase in effective plasma renin activity (EPRA) only by the 70th day of the study. Since oedema preceded any increase in EPRA in some pigs and developed in others without any change in EPRA, it is suggested that the increased renin activity is not responsible for the initial fluid retention and oedema.
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PMID:The effect of protein energy malnutrition on plasma renin and oedema in the pig. 40 33

Renin is found in mouse plasma as high molecular weight forms, in addition to the fully active 40 000 dalton form. By using freshly 125 I-labelled 40 000 dalton pure submaxillary mouse renin, no binding to plasma proteins was demonstrable. However, unfolding and refolding of the labelled renin by guanidine facilitated binding to specific mouse and human plasma proteins. By using antibodies against individual human plasma proteins, the specific binding proteins were identified to be the plasma protease inhibitors: alpha2-macroglobulin, inter-alpha-trypsin inhibitor, alpha2-antithrombin. Binding was also demonstrated to alpha1- and beta1-lipoproteins, albumin and to a non trypsin binding unidentified plasma protein. No binding to 56 other tested proteins was demonstrable. It is concluded that the native 40 000 renin does not bind, but that a conformational change of the renin molecule most likely is necessary before binding occurs. It is discussed whether or not inactive or high molecular weight forms of renin in plasma are 40 000 renin bound to plasma protease inhibitors and lipoprotein.
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PMID:Renin binding proteins in plasma. Binding of renin to some of the plasma protease inhibitors, to lipoproteins, and to a non-trypsin-binding unidentified plasma protein. 42 6

To determine whether acute chloride depletion per se stimulates renin, we produced selective chloride depletion without sodium depletion in rats by peritoneal dialysis (PD) against 0.15 M NaHCO3 or 0.15 M NaNO3. Control rats were dialyzed against 0.15 M NaCl. Plasma renin activity (PRA) was measured before (PRA1) and 105 minutes after (PRA2) PD. Plasma volume was expanded after PD by infusion of salt-free albumin and was measured immediately after PRA2 by [131I]albumin. In experiment 1, rats were prepared on a normal diet. PRA2 (7.0 +/- 1.0 ng/ml per hr, mean +/- SEM) was increased (P less than 0.05) over PRA1 (4.7 +/- 0.7 ng/ml per hr) in Cl-depleted but not in control rats (PRA1 = 5.3 +/- 0.7, PRA2 = 6.1 +/- 0.7, P = NS). In experiment 2, to produce greater chloride depletion, all rats were prepared for 2 weeks on a low salt diet. PRA2 (47 +/- 5 ng/ml per hr) was increased as compared to PRA1 (24 +/- 2 ng/ml per hr, P less than 0.005) in the Cl-depleted group but not in the control group (PRA1 = 24 +/- 3, PRA2 = 27 +/- 6 ng/ml per hr, P = NS). Serum potassium and final plasma volume were slightly but not significantly lower than controls in these Cl-depleted rats. To exclude an additive effect of these two stimuli for renin, in experiment 2a we infused chloride-depleted rats with three times as much albumin as controls and with KHCO3, 100 mEq/liter. Despite volume expansion and potassium loading, PRA2 (41 +/- 6 ng/ml per hr) was significantly elevated as compared to PRA1 (25 +/- 4 ng/ml per hr, P less than 0.01). Since acute metabolic alkalosis also was present in all Cl-depleted renin-stimulated rats, an additional group (2b) was dialyzed against 0.15 M NaNO3; final plasma arterial pH (7.43) was not different from controls (7.42). Nevertheless, PRA2 levels again were higher (36 +/- 6 ng/ml per hr, P less than 0.05) as compared to PRA1 (23 +/- 4 ng/ml per hr). In all experiments, arterial blood pressure, glomerular filtration rate, and filtered sodium load were not different. Free water reabsorption was lower in Cl-depleted than in control rats. We conclude that acute selective chloride depletion per se is a potent stimulus for renin release.
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PMID:Stimulation of renin by acute selective chloride depletion in the rat. 42 74

Arterial plasma levels and hepatic extraction of renin and aldosterone (ALDO) were measured in 24 patients with alcoholic liver disease and in 14 normal subjects being evaluated as prospective kidney donors. Patients with liver disease had higher plasma concentrations and lower fractional hepatic extractions of both renin and ALDO than the normal subjects. The quantity of renin extracted by the liver was highly correlated with plasma renin in both normal subjects and patients. Plasma ALDO concentration was positively correlated with plasma renin (p less than 0.001) but not with serum sodium, potassium or albumin concentration, inferior vena cava pressure, corrected hepatic venous wedge pressure, plasma volume or sulfobromophthalein storage or transport. Sixteen patients were restudied after one month. Six had received 40 mg/day of prednisolone, and the remaining 10 had received a placebo. Neither group had a change in plasma volume, corrected hepatic venous wedge pressure, plasma concentration or hepatic extraction of renin or ALDO. Serum albumin concentration increased and inferior vena cava pressure decreased with prednisolone therapy. These studies document high plasma levels and impaired hepatic extraction of renin and ALDO in patients with liver disease that are not corrected by short-term prednisolone therapy.
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PMID:Plasma levels and hepatic extraction of renin and aldosterone in alcoholic liver disease. 44 56

1. Renin was purified 30 000-fold from rat kidneys by chromatography on DEAE-cellulose and SP-Sephadex, and by affinity chromatography on pepstatinyl-Sepharose. 2. The enzymatic properties of isorenin from rat brain, pseudorenin from hog spleen, cathepsin D from bovine spleen, and renin from rat kidneys were compared: Isorenin, pseudorenin and cathepsin D generate angiotensin from tetradecapeptide renin substrate with pH optima around 4.9, renin at 6.0. With sheep angiotensinogen as substrate, isorenin, pseudorenin and cathepsin D have similar pH profiles (pH optima at 3.9 and 5.5), in contrast to renin (pH optimum at 6.8). 3. The angiotensin-formation from tetradecapeptide by isorenin, pseudorenin and cathepsin D was inhibited by albumin, alpha-and beta-globulins. These 3 enzymes have acid protease activity at pH 3.2 with hemoglobin as the substrate. Renin is not inhibited by proteins and has no acid protease activity. 4. Renin generates angiotensin I from various angiotensinogens at least 100 000 times faster than isorenin, pseudorenin or cathepsin D, and 3000 000 times faster than isorenin when compared at pH 7.2 with rat angiotensinogen as substrate. 5. The 3 'non-renin' enzymes exhibit a high sensitivity to inhibition by pepstatin (Ki less than 5.10(-10) M), in contrast to renin (Ki approximately 6-10(-7) M), at pH 5.5. 6. It is concluded from the data that isorenin from rat brain and pseudorenin from hog spleen are closely related to, or identical with cathepsin D.
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PMID:Isorenin, pseudorenin, cathepsin D and renin. A comparative enzymatic study of angiotensin-forming enzymes. 62 74

The effect of an acute 10% blood volume reduction on plasma renin activity (PRA) was examined in seven patients with minor heart diseases during haemodynamic investigation and in five healthy subjects after 3 days furosemide administration. PRA was not significantly changed. Blood pressure remained constant, atrial pressures decreased. The effect on PRA of an acute 10% blood volume expansion with albumin infusion was studied in thirteen patients with liver or heart diseases. A slight reduction of PRA after albumin did not exceed the expected decrease due to plasma dilution. Blood pressure was unchanged, atrial pressures increased. Renal blood flow increased after albumin in all of the five patients investigated. The effect of PRA of an acute 10% blood volume expansion with whole blood flow increased after albumin in all of the five patients investigated. The effect on PRA of an acute 10% blood volume expansion with whole blood was then investigated in five healthy subjects, pretreated with furosemide for 3 days. A significant decrease in PRA was found. Blood pressure remained constant. It is concluded that an acute blood loss of 10% and an acute blood volume expansion of 10% with albumin have little influence on PRA in supine man, whereas an acute blood volume expansion of 10% with whole blood induces a significant PRA suppression.
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PMID:The influence of acute blood volume changes on plasma renin activity in man. 65 3

1. In four patients with nephrotic syndrome indomethacin not only reduced proteinuria but also inhibited the natriuretic effect of high doses of frusemide. 2. The inhibition of natriuresis by indomethacin could not be antagonized by albumin infusions. 3. Only the combined use of spironolactone and frusemide induced a natriuresis during indomethacin treatment. Spironolactone alone was ineffective. 4. It is suggested that inhibition of prostaglandin synthesis by indomethacin, in the presence of a stimulated renin-angiotensin system and hyperaldosteronism, may cause this strong tendency to sodium retention.
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PMID:Inhibition of frusemide-induced natriuresis by indomethacin in patients with the nephrotic syndrome. 84 48


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