scholarly journals Regulation of atrial natriuretic peptide secretion by a novel Ras-like protein

2007 ◽  
Vol 179 (3) ◽  
pp. 527-537 ◽  
Author(s):  
Igor I. Rybkin ◽  
Mi-Sung Kim ◽  
Svetlana Bezprozvannaya ◽  
Xiaoxia Qi ◽  
James A. Richardson ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Ectopic Expression ◽  
Large Dense Core Vesicles ◽  
Ras Family ◽  
Cellular Machinery ◽  
Endocrine Influence ◽  
Genetic Deletion ◽  
Peptide Secretion ◽  
Atrial Natriuretic

Atrial cardiomyocytes, neurons, and endocrine tissues secrete neurotransmitters and peptide hormones via large dense-core vesicles (LDCVs). We describe a new member of the Ras family of G-proteins, named RRP17, which is expressed specifically in cardiomyocytes, neurons, and the pancreas. RRP17 interacts with Ca2+-activated protein for secretion-1 (CAPS1), one of only a few proteins known to be associated exclusively with LDCV exocytosis. Ectopic expression of RRP17 in cardiomyocytes enhances secretion of atrial natriuretic peptide (ANP), a regulator of blood pressure and natriuresis. Conversely, genetic deletion of RRP17 in mice results in dysmorphic LDCVs, impaired ANP secretion, and hypertension. These findings identify RRP17 as a component of the cellular machinery involved in regulated secretion within the heart and potential mediator of the endocrine influence of the heart on other tissues.

Effect of physical exercise in hypobaric conditions on atrial natriuretic peptide secretion

1992 ◽  
Vol 263 (3) ◽  
pp. R647-R652 ◽  
Author(s):  
O. Vuolteenaho ◽  
P. Koistinen ◽  
V. Martikkala ◽  
T. Takala ◽  
J. Leppaluoto
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Sea Level ◽  
Natriuretic Peptide ◽  
Plasma Renin ◽  
Amino Terminal ◽  
Significant Difference ◽  
Elimination Mechanism ◽  
Peptide Secretion ◽  
Ergometer Test ◽  
Atrial Natriuretic

To evaluate the role of atrial natriuretic peptide (ANP) in exercise-related cardiovascular and hormonal adjustments in hypobaric conditions, 14 young athletes performed a maximal ergometer test in a hypobaric chamber adjusted to simulate the altitudes of sea level and 3,000 m. Plasma immunoreactive ANP levels rose from 5.89 to 35.1 pmol/l at sea level and rose significantly less (P less than 0.05), from 5.36 to 22.3 pmol/l, at simulated 3,000 m. Plasma immunoreactive amino-terminal peptide of proANP (NT-proANP) levels increased to the same extent at sea level and at simulated 3,000 m (from 240 to 481 pmol/l and from 257 to 539 pmol/l, respectively). Plasma immunoreactive aldosterone increased significantly less at simulated 3,000 m (P less than 0.05), but the changes in plasma renin were similar in both conditions. Plasma immunoreactive endothelin-1 and serum erythropoietin levels remained unchanged. In conclusion, we found a blunted ANP response to maximal exercise of ANP in acute hypobaric exposure compared with that in normobaric conditions, but no significant difference in the NT-proANP responses between the two conditions. The divergence may be due to stimulation of the elimination mechanism of ANP.

Potentiation of stretch-induced atrial natriuretic peptide secretion by intracellular acidosis

1999 ◽  
Vol 277 (1) ◽  
pp. H405-H412 ◽  
Author(s):  
Pasi Tavi ◽  
Mika Laine ◽  
Sari Voutilainen ◽  
Petri Lehenkari ◽  
Olli Vuolteenaho ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Imaging System ◽  
Atrial Pressure ◽  
Intracellular Acidosis ◽  
Contraction Force ◽  
Atrial Contraction ◽  
Intracellular Ca ◽  
Peptide Secretion ◽  
Atrial Natriuretic

We sought to investigate whether atrial myocyte contraction and secretion of the atrial natriuretic peptide (ANP) are affected in the same manner by intervention in intracellular Ca2+ handling by acidosis. The effects of propionate (20 mM)-induced intracellular acidosis on the stretch-induced changes in ANP secretion, contraction force, and intracellular Ca2+ concentration ([Ca2+]i) were studied in the isolated rat atrium. The stretch of the atrium was produced by increasing the intra-atrial pressure of the paced and superfused preparation. Contraction force was estimated from pressure pulses generated by the contraction of the atrium. Intracellular Ca2+ was measured from indo 1-AM-loaded atria, and ANP was measured by radioimmunoassay from the perfusate samples collected during interventions. Intracellular pH of the atrial myocytes was measured by a fluorescent indicator (BCECF)-based imaging system. Intracellular acidification caused by 20 mM propionic acid (0.18 pH units) potentiated the stretch-induced (intra-atrial pressure from 1 to 4 mmHg) ANP secretion, causing a twofold secretion compared with nonacidotic controls. Simultaneously, the responsiveness of the atrial contraction to stretch was reduced ( P < 0.05, n = 7). Stretch augmented the systolic indo 1-AM transients in acidic ( P < 0.05, n = 6) and nonacidic atria ( P < 0.05, n = 6). However, during acidosis this was accompanied by an increase of the diastolic indo 1-AM ratio ( P < 0.05, n = 6). Cooccurrence of stretch and acidosis caused an increase in systolic and diastolic [Ca2+]i and potentiated the stretch-induced ANP secretion, whereas the contraction force and its stretch sensitivity were decreased. This mechanism may be involved in ischemia-induced ANP secretion, suggesting a role for ANP secretion as an indicator of contractile dysfunction.

Different Responses of Atrial Natriuretic Peptide Secretion and Its Receptor Density to Salt Intake in Rats

2004 ◽  
Vol 229 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Kyung Sun Lee ◽  
So Young Kim ◽  
Jeong Hee Han ◽  
Yun Ah Kim ◽  
Chunhua Cao ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Salt Intake ◽  
Receptor Density ◽  
Peptide Secretion ◽  
Atrial Natriuretic
Sign in / Sign up

Export Citation Format

Share Document