Cyclic AMP and Sodium Transport: QUANTITATIVE AND TEMPORAL RELATIONSHIPS IN TOAD URINARY BLADDER

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Abstract

The effects of oxytocin upon tissue cAMP content and short-circuit current (SCC) were measured in the urinary bladder of the toad, Bufo marinus. Tissue cAMP levels doubled before any increment in SCC was observed, the two hormone responses were quantitatively related, and a threshold level for an effect of cAMP upon sodium transport was demonstrated. The period of time over which cAMP levels continued to rise after the threshold level had been attained seemed invariant with hormone concentration. The rate at which cAMP levels rose increased with hormone concentration yielding hormone concentration-dependent maximal levels. The decay of cAMP levels was delayed when sodium influx was curtailed, suggesting a sodium-regulatory effect upon tissue cAMP levels.

Authors

Victor S. Sapirstein, Walter N. Scott

Uric Acid: CHARACTERIZATION OF ITS INTERACTION WITH HUMAN SERUM ALBUMIN

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Abstract

Binding of sodium urate to human serum albumin (HSA) was measured by continuous ultrafiltration at pH 7.4 and ionic strength 0.16 over the concentration range 1-13 mg/100 ml. The percent sodium urate bound to 5 g/100 ml HSA was constant over this concentration range: 30.3 (SE±0.6)% being bound at 4°C, 22.6±0.3% at 22.5°C, and 19.6±0.3% at 37°C. Derived association constants, assuming one binding site were 6.0 × 102 M−1 (4°C), 4.47 × 102 M−1 (22.5°C), and 3.88 × 102 M−1 (37°C).

Authors

David S. Campion, Rodney Bluestone, James R. Klinenberg

A Saturable, Vasopressin-Sensitive Carrier for Urea and Acetamide in the Toad Bladder Epithelial Cell

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Abstract

The permeability of the toad bladder to a series of isotopically labeled nonelectrolytes was determined in the presence of 150 mM unlabeled acetamide. Under these conditions, overall bladder function was unimpaired, as shown by a normal response to vasopressin of short-circuit current and permeability coefficient of [3H]water,[14C]ethanol, and [14C]propionamide. The permeability of the bladder to isotopic acetamide and urea, however, was significantly depressed by unlabeled acetamide, in both the absence and presence of vasopressin. These experiments indicate a competition between unlabeled and isotopic species for binding sites, and show the existence of a saturable, vasopressin-sensitive carrier for urea and acetamide in the epithelial cell membrane.

Authors

Sherman Levine, Nicholas Franki, Richard M. Hays

Heterogeneity of 5′-Nucleotidase Activity in Lymphocytes in Chronic Lymphocytic Leukemia

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Abstract

The specific activity of 5′-nucleotidase was determined in lymphocyte plasma membranes from 14 normal subjects and 10 patients with chronic lymphocytic leukemia (CLL). Whereas the enzyme was present in the preparation from normal lymphocytes, in 7 out of 10 CLL patients the membranes had markedly decreased or no detectable 5′-nucleotidase activity. The lack of this activity from the lymphocytes of most patients with CLL constitutes an alteration in a plasma membrane enzyme from the normal cell. The presence of the enzyme in the lymphocytes of some patients with CLL and its decrease in others provide further evidence for biochemical heterogeneity among patients with this disorder.

Authors

John Lopes, Dorothea Zucker-Franklin, Robert Silber

Evidence for Stimulation of Renal Gluconeogenesis by Catecholamines

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Abstract

Isoproterenol and norepinephrine (10-4 M) significantly increased cyclic AMP formation and glucose production by the isolated tubules of the renal cortex of the rat. These effects were abolished by propranolol. Theophylline diminished the effects of the catecholamines on gluconeogenesis despite a marked augmentation in cyclic AMP concentration. In the absence of calcium ion in the incubation medium, isoproterenol stimulates cyclic AMP production, but has no effect on gluconeogenesis. It is concluded that catecholamines enhance gluconeogenesis in renal cortical tubules by the stimulation of beta adrenergic receptors. This effect is probably mediated through adenyl cyclase-cyclic AMP system and requires an adequate level of ATP and the presence of calcium ion.

Authors

Kiyoshi Kurokawa, Shaul G. Massry

Formation of Prostaglandins during the Aggregation of Human Blood Platelets

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Abstract

Prostaglandins E2 and F2α were formed in response to ADP, L-epinephrine, or collagen by human platelets suspended in plasma containing citrate anticoagulant and stirred at 37°C. The prostaglandins formed by platelets in response to collagen were rapidly released and the amounts formed were proportional to the amount of collagen added. The formation of the prostaglandins was associated with the single wave of aggregation induced by collagen or the second wave of aggregation induced by epinephrine. The above findings are discussed with reference to published studies on the biochemical changes occurring during platelet aggregation. It is suggested that the formation and release of prostaglandins is associated with the secretion of endogenous ADP and 5-hydroxytryptamine.

Authors

J. B. Smith, Carol Ingerman, J. J. Kocsis, M. J. Silver

Dietary-Induced Variation of Hypoxanthine-Guanine Phosphoribosyl Transferase Activity in Patients with the Lesch-Nyhan Syndrome

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Abstract

We have studied three patients with the Lesch-Nyhan syndrome to assess the effect of dietary purines on erythrocyte hypoxanthine-guanine phosphoribosyltransferase (HGPRT) activity. During dietary purine restriction HGPRT activity rose in all three patients; resumption of normal dietary purine intake or the addition of adenine (10 mg/kg per day) to a purinefree diet resulted in a fall in HGPRT activity. These changes in enzyme activity appeared to be due to an activation or inactivation of the mutant enzyme without a change in the half-life or absolute amount of HGPRT enzyme protein.

Authors

William J. Arnold, William N. Kelley

Biological Defense Mechanisms. THE PRODUCTION BY LEUKOCYTES OF SUPEROXIDE, A POTENTIAL BACTERICIDAL AGENT

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Abstract

As a highly reactive substance produced in biological systems by the one-electron reduction of oxygen, superoxide (O2-) seemed a likely candidate as a bactericidal agent in leukocytes. The reduction of cytochrome c, a process in which O2- may serve as an electron donor, was found to occur when the cytochrome was incubated with leukocytes. O2- was identified as the agent responsible for the leukocyte-mediated reduction of cytochrome c by the demonstration that the reaction was abolished by superoxide dismutase, an enzyme that destroys O2-, but not by boiled dismutase, albumin, or catalase.

Authors

Bernard M. Babior, Ruby S. Kipnes, John T. Curnutte

Autonomous Erythropoiesis during Erythroblastic Crisis of Chronic Myelocytic Leukemia

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Abstract

Two patients with chronic myelocytic leukemia who developed an erythroblastic rather than a myeloblastic phase were studied with respect to whether or not the megaloblastic erythropoiesis was subject to normal control mechanisms. After transfusion, no significant reduction was observed in the percentage of nucleated erythroid precursors or of proerythroblasts in marrow or in blood reticulocytes. In one of the two patients, ferrokinetics and urinary erythropoietin levels were studied and were also compatible with the conclusions that erythropoiesis was autonomous in this rare syndrome. Three patients with clinical pictures compatible with Di Guglielmo's syndrome were studied as controls. As has been reported previously, erythropoiesis in this syndrome appeared to be responsive to normal control mechanisms. These data suggest that these two clinically similar syndromes, erythroblastic crisis of chronic myelocytic leukemia and Di Guglielmo's syndrome may represent qualitatively different defects in hematopoietic stem cells.

Authors

C. H. Srodes, E. H. Hyde, D. R. Boggs

Deficiency of the Chemotactic Factor Inactivator in Human Sera with α₁-Antitrypsin Deficiency

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Abstract

As revealed by appropriate fractionation procedures, human serum deficient in α1-antitrypsin (α1-AT) is also deficient in the naturally occurring chemotactic factor inactivator. These serum donors had severe pulmonary emphysema. Serum from patients with clinically similar pulmonary disease, but with presence of α1-AT in the serum, showed no such deficiency of the chemotactic factor inactivator. When normal human serum and α1-AT-deficient human sera are chemotactically activated by incubation with immune precipitates, substantially more chemotactic activity is generated in α1-AT-deficient serum. These data indicate that in α1-AT-deficient serum there is an imbalance in the generation and control of chemotactic factors. It is suggested that the theory regarding development of pulmonary emphysema in patients lacking the α1-antitrypsin in their serum should be modified to take into account a deficiency of the chemotactic factor inactivator.

Authors

Peter A. Ward, Richard C. Talamo