scholarly journals Getting a G–RRP on regulated exocytosis in the heart

2007 ◽  
Vol 179 (3) ◽  
pp. 371-373 ◽  
Author(s):  
Christopher C. Glembotski
Keyword(s):  
Skeletal Muscle ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Peptide Hormone ◽  
Secretory Cells ◽  
Related Protein ◽  
Atrial Myocytes ◽  
Regulated Exocytosis ◽  
Regulated Secretion ◽  
New Protein

A study by Rybkin et al. (see p. 527) substantially advances our understanding of regulated exocytois by specialized secretory cells, such as atrial myocytes. A second member of the Ras-related protein family, RRP17, was identified and shown to participate in regulating the secretion of the cardiac-derived peptide hormone, atrial natriuretic peptide. In addition to the heart, RRP17 was shown to be expressed in neuronal, pancreatic, and skeletal muscle cells, suggesting a widespread role in regulated secretion for this new protein.

Atrial pressure, distension, and pacing frequency in ANP secretion in isolated perfused rabbit atria

1991 ◽  
Vol 260 (1) ◽  
pp. R39-R46 ◽  
Author(s):  
K. W. Cho ◽  
K. H. Seul ◽  
S. H. Kim ◽  
K. M. Seul ◽  
G. Y. Koh
Keyword(s):  
Electrical Stimulation ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Pressure ◽  
Atrial Pacing ◽  
Atrial Myocytes ◽  
Volume Changes ◽  
Series Of Experiments ◽  
The Relationship ◽  
Rabbit Atria

It has been suggested in this laboratory that the principal stimulus for the secretion of atrial natriuretic peptide (ANP) is the reduction of atrial distension and that the secretion of ANP is dependent on both atrial reduction volume and reduction frequency. To investigate the relationship among the changes in atrial pressure, distension, pacing frequency, and ANP secretion, we performed a series of experiments in the isolated perfused rabbit atria. Increase in atrial pressure without changes in transmural pressure and thus without volume changes did not raise immunoreactive ANP (irANP) secretion. Atrial distension without changes in intracavitary atrial pressure increased irANP secretion with the reduction. Electrical stimulation with atrial distension resulted in an increase in irANP secretion in proportion to pacing frequency. Incremental response of irANP secretion to electrical stimulation was accentuated by increasing atrial distension. Neither atrial pacing without distension nor distension without pacing raised irANP secretion. These results suggest that the direct and principal stimulus for irANP secretion in response to atrial pacing and distension is the length shortening of atrial myocytes and that the incremental response of irANP secretion to increasing pacing frequency is the result of an increase in frequency of the length shortening of atrial myocytes.

Hormonal Control of Atrial Natriuretic Peptide Synthesis and Secretion from Cultured Atrial Myocytes

1993 ◽  
Vol 25 (5) ◽  
pp. 509-518 ◽  
Author(s):  
Thomas M. Muir ◽  
Jane Hair ◽  
Gordon C. Inglis ◽  
Jocelyn W. Dow ◽  
George B.M. Lindop ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Peptide Synthesis ◽  
Hormonal Control ◽  
Atrial Myocytes ◽  
Atrial Natriuretic

Pro-atrial natriuretic peptide hormone from right atria is correlated with cardiac depression in septic patients

2001 ◽  
Vol 24 (7) ◽  
pp. RC22-RC24 ◽  
Author(s):  
Branka Mazul-Sunko ◽  
N. Zarkovic ◽  
N. Vrkic ◽  
R. Klinger ◽  
M. Peric ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Peptide Hormone ◽  
Cardiac Depression ◽  
Right Atria ◽  
Atrial Natriuretic

Effects of ANP receptor antagonists on ANP secretion from adult rat cultured atrial myocytes

1995 ◽  
Vol 268 (3) ◽  
pp. E428-E432 ◽  
Author(s):  
S. Nachshon ◽  
O. Zamir ◽  
Y. Matsuda ◽  
N. Zamir
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Guanylyl Cyclase ◽  
Second Messenger ◽  
Target Cells ◽  
Atrial Myocytes ◽  
Receptor Antagonists ◽  
Adult Rat ◽  
Cgmp Formation ◽  
Autoregulatory Mechanism

Atrial natriuretic peptide (ANP) is a hormone-secreted predominantly by atrial myocytes. ANP exerts many of its actions via activation of the particulate guanylyl cyclase receptor ANPR-A and the formation of guanosine 3',5'-cyclic monophosphate (cGMP), which serves as a second messenger in the target cells. Using membrane-permeable cGMP analogues (8-bromo-cGMP and dibutyryl- cGMP), we first tested the hypothesis that ANP secretion by adult rat cultured atrial myocytes can be modulated through the second messenger cGMP. Second, we examined the effects of two competitive ANPR-A receptor antagonists, namely HS-142-1 and anantin, on cGMP formation and ANP secretion from cultured atrial myocytes. Cultured atrial myocytes secreted large quantities of immunoreactive (ir) ANP under basal conditions. We found that cGMP analogues inhibited basal irANP secretion from cultured atrial myocytes, whereas HS-142-1 and anantin had stimulating effects. HS-142-1 and anantin reduced cGMP formation in cultured atrial myocytes at basal conditions. These results suggest an autoregulatory mechanism of ANP secretion by atrial myocytes in an autocrine/paracrine fashion.

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