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

scholarly journals Expression and Secretion of an Atrial Natriuretic Peptide in Beige-Like 3T3-L1 Adipocytes

2019 ◽  
Vol 20 (24) ◽  
pp. 6128 ◽  
Author(s):  
In-Seon Bae ◽  
Sang Hoon Kim
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Peptide Hormone ◽  
Brown Adipocyte ◽  
Omega 3 ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Beige Adipocytes ◽  
Atrial Natriuretic

The browning of white adipose tissue (beige adipocytes) stimulates energy expenditure. Omega-3 fatty acids have been shown to induce thermogenic action in adipocytes via G-protein coupled receptor 120 (GPR120). Atrial natriuretic peptide (ANP) is a peptide hormone that plays the role of maintaining normal blood pressure in kidneys to inhibit Na+ reuptake. Recently, ANP was found to induce adipocyte browning by binding to NPR1, an ANP receptor. However, the expression of ANP in adipocytes has not yet been studied. Therefore, in this study, we investigate the expression of ANP in beige-like adipocytes induced by docosahexaenoic acids (DHA), T3, or a PPAR agonist, rosiglitazone. First, we found that brown adipocyte-specific genes were upregulated in beige-like adipocytes. DHA promoted ANP expression in beige-like cells, whereas DHA-induced ANP expression was abolished by GPR120 knockout. ANP secretion of beige-like adipocytes was increased via PKC/ERK1/2 signaling in the GPR120 pathway. Furthermore, ANP secreted from beige-like adipocytes acted on HEK-293 cells, the recipient cells, leading to increased cGMP activity. After the NPR1 knockdown of HEK-293 cells, cGMP activity was not changed. Taken together, our findings indicate that beige-like adipocytes induce ANP secretion, which may contribute to improving obesity-associated metabolic disease.

Cardiac and plasma atrial natriuretic peptide after 9-day hindlimb suspension in rats

1994 ◽  
Vol 76 (2) ◽  
pp. 641-649 ◽  
Author(s):  
J. Fareh ◽  
B. Bayard ◽  
J. Gabrion ◽  
G. Thibault ◽  
J. Oliver ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Mrna Expression ◽  
Natriuretic Peptide ◽  
Hindlimb Suspension ◽  
Dense Granules ◽  
Atrial Cardiocytes ◽  
Male Wistar Rats ◽  
The Right ◽  
Right Atria ◽  
Atrial Natriuretic

To determine atrial natriuretic peptide (ANP) adaptation to simulated weightlessness, immunoreactive plasma (ir-NH2- and ir-COOH-terminals) and atrial (ir-COOH-terminal) ANP levels, atrial mRNA expression, immunoreactive cardiocyte ANP levels (ir-NH2- and ir-COOH-terminals), and ultrastructural observations of granules in atrial cardiocytes were assessed in male Wistar rats after a 9-day hindlimb suspension. Plasma ir-NH2- and ir-COOH-terminal ANP concentrations decreased by 17 (P < 0.05) and 37% (P < 0.05), respectively, in suspended rats. A concomitant ir-COOH-terminal ANP content reduction was also observed in left (31%; P < 0.01) and right atria (25%; P < 0.05). Atrial ANP mRNA expression was severely depleted in the right atrium and less so in the left atrium after 9 days of hindlimb suspension. Immunocytochemistry observations demonstrated lowered NH2- and COOH-terminal ANP immunoreactivities in left and right atria from suspended rats. A reduced number of storage granules (dense granules) in both atria was also noted on ultrastructural analysis. It was concluded that ANP biosynthesis, storage, and release were decreased after a 9-day hindlimb suspension.

Mechanisms of isoproterenol-induced atrial natriuretic peptide release from superfused rabbit atria

1993 ◽  
Vol 265 (4) ◽  
pp. H1283-H1288 ◽  
Author(s):  
C. Azizi ◽  
A. Carayon ◽  
F. Masson ◽  
E. Noe ◽  
C. Barthelemy ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Calcium Concentration ◽  
Extracellular Calcium ◽  
Beta Agonist ◽  
Cyclic Monophosphate ◽  
Peptide Release ◽  
Right Atria ◽  
Rabbit Atria ◽  
Atrial Natriuretic

The mechanisms for isoproterenol-induced atrial natriuretic peptide (ANP) release were studied in superfused rabbit sliced right atria. Addition of 1 microM norepinephrine to this preparation induced a significant monophasic twofold rise in ANP release. This effect was abolished by 1 microM propranolol and mimicked by 1 microM isoproterenol. Furthermore, addition of 200 microM 3-isobutyl-1-methylxanthine (IBMX) to the superfusing medium potentiated isoproterenol effect 31%. In addition, superfusion of slices with 0.5 mM N6,2-O-dibutyryladenosine 3',5'-cyclic monophosphate [(Bu)-2cAMP] enhanced ANP release in the same manner as the beta-agonist. After isoproterenol stimulation, adenosine 3',5'-cyclic monophosphate (cAMP) concentration in effluents increased significantly. ANP secretory response to isoproterenol was unaffected by extracellular calcium concentration or 1 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). Finally, 10 microM indomethacin significantly reduced isoproterenol-stimulated ANP release. It is concluded that 1) norepinephrine-induced ANP release is mediated by its beta-agonist activity, 2) isoproterenol-stimulated release appears to be mediated by cAMP, 3) isoproterenol effect does not require extracellular calcium, and 4) prostaglandins may be involved in this beta-adrenergic effect.

scholarly journals Regulation of atrial natriuretic peptide (ANP) and its role in blood pressure

2012 ◽  
Vol 1 (7) ◽  
pp. 176-179 ◽  
Author(s):  
Feroz Ahmed ◽  
Nahida Tabassum ◽  
Saima Rasool
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Renin Angiotensin System ◽  
Peptide Hormone ◽  
Decompensated Heart Failure ◽  
Pharmaceutical Journal ◽  
The Body ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) a powerful vasodilator, and a protein (28-amino acid peptide) hormone secreted by heart muscle cells. It is released in response to atrial distention, stretching of the vessel walls, sympathetic stimulation of ?-adrenoceptors, raised sodium concentration, angiotensin-II and endothelin. ANP binds to three cell surface receptors called ANP receptors. The overall effect of ANP on the body is to counter increases in blood pressure and volume caused by the renin-angiotensin system. It has also been reported to increase the release of free fatty acids from adipose tissue. Regulation of its effects is achieved through gradual degradation of the peptide by the enzyme neutral endopeptidase (NEP). Inhibitors of NEP are currently being developed to treat disorders ranging from hypertension to heart failure. Synthetic analogs of ANP have been investigated as potential therapies for the treatment of decompensated heart failure and other diseases.DOI: http://dx.doi.org/10.3329/icpj.v1i7.10812International Current Pharmaceutical Journal 2012, 1(7): 176-179 

scholarly journals Light and electron microscopic localization of atrial natriuretic peptide in the heart of spontaneously hypertensive rat.

1988 ◽  
Vol 36 (10) ◽  
pp. 1239-1249 ◽  
Author(s):  
J A Gu ◽  
L Gonzalez-Lavin
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Spontaneously Hypertensive Rat ◽  
Peptide Hormone ◽  
Electron Microscopic Level ◽  
Hypertensive Rats ◽  
Electron Microscopic ◽  
Spontaneously Hypertensive ◽  
Specific Granules ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) is a newly discovered peptide hormone present mainly in the atria. We investigated the occurrence and distribution of ANP immunoreactivity in the myocardiocytes of the ventricles of spontaneously hypertensive rats by use of immunocytochemistry at both light and electron microscopic level. ANP immunoreactivity was found in the specific granules in the cytoplasm of the cardiocytes in the subendocardium and the myocardium of the ventricles, as well as in the atria. The specific granules found in the ventricles of hypertensive rats were similar in size, shape, and ANP immunoreactive content to those in the atria. The abundance of ANP immunoreactivity in the left ventricle is greater than that in the right, and appears to increase with increasing severity of hypertension. Conversely, the overall content of ANP in the atria of hypertensive rats was decreased when compared with that in age-matched normotensive rats. The present findings indicate that ventricles may become a major source for ANP synthesis and release during hypertension, and may play important roles in cardiac endocrine pathology and cardiac hypertrophy.

Synthesis and secretion of atrial natriuretic peptide by BON cells: Stimulation by PMA and cGMP

2001 ◽  
Vol 120 (5) ◽  
pp. A682-A682
Author(s):  
W GOWERJR ◽  
G CARTER ◽  
C LANDON ◽  
W GOWERIII ◽  
J DIETZ ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Bon Cells ◽  
Atrial Natriuretic
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