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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 63 (1985), S. 529-536 
    ISSN: 1432-1440
    Keywords: Atrial natriuretic factor ; Cyclic GMP ; Diuresis ; Vasorelaxation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ever since the early work of Henry and Gauer (1956) it has been clear that a link exists between the atria of mammals and diuresis. In 1981, De Bold et al. described that atrial extracts, injected intravenously into rats, caused diuresis. The hormone responsible for this diuresis has quickly been identified. The peptide hormone, atrial natriuretic factor (ANF), which is also known as atrial natriuretic peptide(s) (ANP), cardionatrin, cardiodilatin, atrin or auriculin, has been sequenced and synthetically produced. Its genomic DNA has been cloned. ANF raises cyclic GMP in target cells and activates particulate guanylate cyclase but not soluble guanylate cyclase. So far, no other hormone has conclusively been shown to activate particulate guanylate cyclase. ANF is formed and secreted in the atria but not in the ventricles of mammals, including man. The action of ANF involves natriuresis, vasorelaxation and inhibition of aldosterone secretion. ANF or ANF derivatives may represent a therapeutically useful new class of agents.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Atrial natriuretic peptide ; Cyclic GMP ; Volume loading
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the effects of fluid expansion on endogenous atrial natriuretic peptide (ANP) and cyclic 3′,5′-guanosine monophosphate (cGMP), four male volunteers were studied before, during and after intravasal volume loading. Volume expansion was performed by intravenous infusion of 2,000 ml isotonic saline solution within 30 min. Mean plasma ANP levels increased 2.5-fold from 31.2 pg/ml to 81.7 pg/ml 40 min after the start of infusion. Plasma cGMP levels paralleled the rise in ANP, shwoing a mean cGMP increment from 2.7 pmol/ml to a maximum of 8.2 pmol/ml. Both ANP and cGMP levels were back to basal levels 120 min after termination of the infusion. Stimulation of endogenous ANP release by volume loading suggests that ANP is involved in the regulation of fluid homeostasis in man. The parallel rise in plasma cGMP levels supports the idea that cGMP is a mediator for the effects of ANP.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0014-5793
    Keywords: Cyclic GMP ; Guanylate cyclase ; Guanylin ; Hemofiltrate ; Peptide hormone
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0014-5793
    Keywords: Atrial natriuretic factor ; Cyclic GMP ; Glomerulus ; Particulate guanylate cyclase ; Sodium nitroprusside ; Tubule
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1440
    Keywords: Cyclic GMP ; Atrial natriuretic factor ; Platelets ; Receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Thirty-seven patients with volume-retaining disorders (liver cirrhosis with ascites,n=8; heart failure NYHA III–IV,n=12; endstage renal failure,n=17) and twelve healthy age-matched controls were given a small dose (33 μg) of hANF (human atrial natriuretic factor). We tested the resulting hemodynamic and renal effects as well as the effect on plasma cyclic GMP levels and compared them with the properties of platelet ANF receptors. The ANF injection evoked an increase in cyclic GMP plasma levels of 19.3±2.2 nM in healthy controls. This increase tended to be smaller in the cirrhosis group (15.5±3.3 nM) and in the heart failure group (16.8±2.3 nM) than in the dialysis group (20.5±2.5 nM). The invasion rates of cyclic GMP were comparable in all groups, but the evasion rates increased more in the heart failure and endstage renal failure groups (27.9±7.7 min and 26.1±3.4 min, respectively) than in the cirrhosis and control groups (14.9±1.9 min and 14.2±1.9 min, respectively). Patients with endstage renal failure and congestive heart failure showed a smaller decrease in diastolic blood pressure than controls and patients with liver cirrhosis. Renal actions of ANF were diminished in cirrhosis and heart failure patients. Binding capacities of platelet ANF receptors were higher in the control group (12.2±1.5 receptors/cell) than in the patient groups (cirrhosis, 7.8±1.2; endstage renal failure, 8.0±0.9; heart insufficiency, 8.0±1.0 receptors/ cell), with no differences among the patient groups. Binding affinities were not significantly different. Correlation analysis showed that the relationship between the actions of ANF and the increases in plasma cyclic GMP levels is loose and cannot predict the hemodynamic or renal effects of exogenous ANF in a given patient. Although the behavior of plasma cyclic GMP levels fails to predict the responsiveness of the body to ANF in a given patient, it does reflect the differences between the patient groups and the control group. In contrast, we found no correlation between the properties of platelet ANF receptors and ANF action.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1440
    Keywords: Molsidomine ; SIN 1 ; Guanylate cyclase ; Cyclic GMP ; Platelet aggregation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To find out whether 3-morpholino-sydnonimine (SIN 1), the active metabolite of molsidomine, exerts its antiaggregatory effects not only in vitro but also in vivo, we tested ex vivo aggregation before and after intravenous application of molsidomine in healthy volunteers. We also measured plasma levels of guanosine 3′∶5′-cyclic monophosphate (cyclic GMP) as SIN 1, the bioactive metabolite of molsidomine, becomes effective via activation of soluble guanylate cyclase. In eight out of ten subjects molsidomine had an inhibitory effect on platelet aggregation and a higher threshold concentration of platelet-activating factor was required after molsidomine application to induce irreversible aggregation. Despite the effect on platelets, plasma cyclic GMP levels did not increase. These results suggest that the nitric oxide-containing SIN 1 inhibits platelet aggregation not only in vitro but also in vivo and that this property can be a beneficial effect in antianginal therapy.
    Type of Medium: Electronic Resource
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