Noncalcium-Dependent Modulation of in Vitro Atrial Natriuretic Factor Release by Extracellular Osmolality*

Endocrinology ◽  
1987 ◽  
Vol 120 (1) ◽  
pp. 194-197 ◽  
Author(s):  
DANIEL M. GIBBS
Keyword(s):  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
Factor Release ◽  
Atrial Natriuretic

Effect of manipulations of Ca2+ environment on atrial natriuretic factor release

1989 ◽  
Vol 256 (6) ◽  
pp. H1588-H1594 ◽  
Author(s):  
M. L. De Bold ◽  
A. J. De Bold
Keyword(s):  
Atrial Natriuretic Factor ◽  
Mechanical Activity ◽  
Apparent Effect ◽  
Natriuretic Factor ◽  
Atrial Cardiocytes ◽  
Free Media ◽  
Kinetics Of ◽  
Factor Release ◽  
Atrial Natriuretic

The effects of Ca2+ on the kinetics of atrial natriuretic factor (ANF) release [measured as immunoreactive cardionatrin (IRC)] were studied on an in vitro, spontaneously beating rat atrial preparation. It was found that ethylene glycolbis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) and Ca2+-free media induced a significant increase in the rate of basal IRC release. Reintroduction of Ca2+ reversed the augmented basal IRC release induced by EGTA and restored mechanical activity. It was also found that the stretch-induced IRC release was independent of extracellular Ca2+ and took place even in the presence of EGTA. The presence of absence of Ca2+ had no apparent effect on ANF processing. In all instances, cardionatrin I (ANF 99-126) was found to be the most abundant peptide released. Morphologically, no obvious differences were observed during either basal or stretch-induced IRC release. These results suggest that, unlike most other endocrine secretory systems, a reduction of cytosolic Ca2+ stimulates basal IRC release. These findings suggest an adaptation of atrial cardiocytes to accomplish their dual role as secretory and contractile cells.

Endotoxin-induced atrial natriuretic factor release: In vivo and in vitro studies

1998 ◽  
Vol 179 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Papineni S. Rao ◽  
Denis Cavanagh ◽  
Lloyd B. Graham ◽  
John R. Dietz ◽  
James V. Fiorica ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
In Vitro Studies ◽  
Natriuretic Factor ◽  
Factor Release ◽  
Atrial Natriuretic

Thirty years of research on atrial natriuretic factor: historical background and emerging concepts

2011 ◽  
Vol 89 (8) ◽  
pp. 527-531 ◽  
Author(s):  
Adolfo J. de Bold
Keyword(s):  
Atrial Natriuretic Factor ◽  
Hybrid Approach ◽  
Biological Properties ◽  
Historical Background ◽  
Endocrine Function ◽  
Intracellular Targeting ◽  
Natriuretic Factor ◽  
Polypeptide Hormones ◽  
Atrial Natriuretic

The discovery of the natriuretic properties of atrial muscle extracts pointed to the existence of an endocrine function of the heart that is now known to be mediated by the polypeptide hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP). On the basis of such a finding, approximately 27 000 publications to date have described a wide variety of biological properties of the heart hormones as well as their application as therapeutic agents and biomarkers of cardiac disease. Stimulation of secretion of ANF and BNP from the atria is mediated through mechanisms involving G proteins of the Gq or Go types. We showed that the latter type underlies the transduction of muscle stretch into stimulated secretion and that it is more highly abundant in atria than in ventricles. The Gαo-1 subunit appears to play a key role in the biogenesis of atrial granules and in the intracellular targeting of their contents. Protein interaction studies using a yeast two-hybrid approach showed interactions between Gαo-1, proANF, and the intermediate conductance, calcium-activated K+ channel SK4. Pharmacological inhibition of this channel decreases ANF secretion. Unpublished studies using in vitro knockdowns suggest interdependency in granule protein expression levels. These studies suggest previously unknown mechanisms of intracellular targeting and secretion control of the heart hormones that may find an application in the therapeutic manipulation of circulating ANF and BNP.

The Action of Atrial Natriuretic Factor on Glomerular Diameter in Vitro

1988 ◽  
Vol 529 (1 Fourth Colloq) ◽  
pp. 175-177
Author(s):  
WARREN L. ROSENBERG ◽  
CHRISTOPHER V. KEOGH ◽  
BEVERLY A. HALL ◽  
LUIGI ALBANO
Keyword(s):  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Atrial natriuretic factor binding sites in the jejunum

1989 ◽  
Vol 256 (2) ◽  
pp. G436-G441 ◽  
Author(s):  
C. Bianchi ◽  
G. Thibault ◽  
A. De Lean ◽  
J. Genest ◽  
M. Cantin
Keyword(s):  
Binding Sites ◽  
Atrial Natriuretic Factor ◽  
Specific Binding ◽  
Rat Tissues ◽  
Rat Jejunum ◽  
Specific Binding Sites ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

We have studied the localization and the characterization of atrial natriuretic factor (ANF) binding sites by radioautographic techniques. Quantitative in vitro radioautography with a computerized microdensitometer demonstrated the presence of high-affinity, low-capacity 125I-ANF-(99-126) binding sites (Kd, 48 pM; Bmax, 63 fmol/mg protein) mainly in the villi of 20-microns slide-mounted transverse sections of the rat jejunum. Competition curves showed 50% inhibitory concentrations of 55 and 1,560 pM for ANF-(99-126) and ANF-(103-123), respectively. In vivo electron microscope radioautography showed that 80% of the silver grains were localized on the lamina propria fibroblast-like cells, 18% on mature enterocytes, and 2% on capillaries. Bradykinin and adrenocorticotropin did not compete with ANF binding. These results demonstrate that ANF binding sites in the rat jejunum possess the pharmacological characteristics of functional ANF receptors encountered in other rat tissues, and ultrastructural radioautographs show their cellular distribution. Taken together, these results demonstrate the presence and the localization of specific binding sites for ANF in the jejunal villi of the rat small intestine.

In vitro secretion of atrial natriuretic factor: receptor-mediated release of prohormone

1988 ◽  
Vol 254 (5) ◽  
pp. R809-R814 ◽  
Author(s):  
A. T. Veress ◽  
S. Milojevic ◽  
C. Yip ◽  
T. G. Flynn ◽  
H. Sonnenberg
Keyword(s):  
Atrial Natriuretic Factor ◽  
Active Form ◽  
High Concentration ◽  
Natriuretic Factor ◽  
Rat Hearts ◽  
Agonist Concentration ◽  
Atrial Natriuretic Factor Receptor ◽  
Atrial Natriuretic

Secretion of atrial natriuretic factor (ANF) in vivo is thought to be mediated by atrial distension. We have shown previously that nonstretched atria can release natriuretic activity in vitro when stimulated by certain agonists. In the present study atrial appendages from freshly excised rat hearts were incubated at 37 degrees C for up to 1 h in the presence of either vasopressin (5 X 10(-9) mol/l) or angiotensin II (2.5 X 10(-7) mol/l). Aliquots of postincubation media were injected intravenously into anesthetized bioassay rats to determine natriuretic activity. Control media, in which atria had been incubated without agonist, did not cause natriuresis. Significant increases in sodium excretion were seen after injection of media in which atria had been incubated in the presence of either agonist. Injection of medium with the same agonist concentration did not result in comparable natriuresis. Radioimmunoassay (RIA) indicated a high concentration of immunoactive ANF in the natriuretic media. However, radioreceptor assay (RRA) of the same media gave apparent ANF concentrations that were lower by about three orders of magnitude. Because the antibody used in the RIA cross reacts with ANF prohormone, whereas the RRA is sensitive only to the active form, we concluded that agonist-induced, stretch-independent release of ANF is in the form of prohormone, which can be converted to the active hormone in the circulation of the bioassay animal. The conclusion of prohormone release was confirmed by liquid chromatography. The data thus suggest that receptor-mediated as well as stretch-induced ANF secretion may be important in regulating the activity of the ANF system.

Downregulation of atrial natriuretic factor clearance receptors in experimental chronic renal failure rats

1995 ◽  
Vol 269 (3) ◽  
pp. H902-H908 ◽  
Author(s):  
J. K. Luk ◽  
E. F. Wong ◽  
N. L. Wong
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Atrial Natriuretic Factor ◽  
Radioligand Binding ◽  
High Plasma ◽  
Natriuretic Factor ◽  
Clearance Receptor ◽  
Acid Wash ◽  
Atrial Natriuretic

Studies were performed to examine the changes of renal ANF second messenger guanosine 3',5'-cyclic monophosphate (cGMP) responses and receptor properties in chronic renal failure (CRF). Five-sixths-nephrectomized and sham-operated Wistar rats were used. The glomerular filtration rate was decreased in the five-sixths-nephrectomized rats, which also had significantly higher plasma blood urea nitrogen and plasma atrial natriuretic factor (ANF) levels (148.5 +/- 10.2 vs. 115.7 +/- 7.3 pg/ml, P = 0.01) than the sham rats. In vitro ANF-stimulated cGMP accumulations in glomeruli of five-sixths-nephrectomized rats were higher than controls. Radioligand-binding experiments showed downregulation of the total ANF receptor in both acid and nonacid wash CRF glomeruli (nonacid wash: 189 +/- 25 vs. 362.8 +/- 52.8 fmol/mg protein, P < 0.05; acid wash: 449.8 +/- 67 vs. 652.7 +/- 52.5 fmol/mg protein, P < 0.05). No change in receptor densities was observed in the des(Gln18,Ser19,Gly20,Leu21)atrial natriuretic peptide-(4--23)-NH2-resistant receptors between sham and CRF rat glomeruli. Therefore, downregulation of ANF clearance receptors exists in CRF rat glomeruli, and this is associated with the exaggerated ANF-stimulated cGMP response in these CRF glomeruli. Hypersensitivity of CRF rat to ANF, together with high plasma ANF levels and downregulation of clearance receptor, may contribute to increased sodium excretion in CRF.

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