scholarly journals Protein kinase C-dependent prostaglandin production mediates angiotensin II-induced atrial-natriuretic peptide release

1994 ◽  
Vol 298 (2) ◽  
pp. 451-456 ◽  
Author(s):  
D J Church ◽  
S Braconi ◽  
V van der Bent ◽  
M B Vallotton ◽  
U Lang
Keyword(s):  
Protein Kinase C ◽  
Angiotensin Ii ◽  
Protein Kinase ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Ang Ii ◽  
Rat Cardiomyocytes ◽  
Kinase C ◽  
Alpha Production ◽  
Atrial Natriuretic

The respective roles of protein kinase C (PKC) and endogenous prostaglandin formation in angiotensin II (Ang II)-induced myocardial secretion of atrial natriuretic peptide (ANP) was studied in cultured, spontaneously beating, neonatal-rat cardiomyocytes. Incubation of cardiomyocytes with 0.1 microM Ang II led to a rapid but transient increase in particulate-bound PKC activity, a response accompanied by marked increases in cellular 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) generation and ANP secretion. A role for PKC in Ang II-induced 6-oxo-PGF1 alpha formation and ANP secretion was apparent, insofar as both responses were suppressed in the presence of the PKC inhibitors staurosporine (1 microM) and CGP 41251 (1 microM), as well as in cells in which PKC had been previously down-regulated by pretreatment with phorbol diester. Furthermore, Ang II-induced 6-oxo-PGF1 alpha production was found to be strongly correlated with Ang II-induced ANP release (r = 0.87, P < 0.001, n = 6), indicating a role for prostacyclin (PGI2) in Ang II-induced ANP secretion in these cells. This hypothesis was confirmed by finding that both Ang II-induced 6-oxo-PGF1 alpha production and ANP release were abolished in the presence of the respective phospholipase A2 and cyclo-oxygenase inhibitors quinacrine (10 microM) and indomethacin (10 microM), whereas exogenously applied PGI2 (1 microM) and prostaglandin E2 (0.1 microM) mimicked Ang II-induced ANP secretion in this system. Taken together, these results suggest that Ang II induces ANP secretion in spontaneously beating rat cardiomyocytes via a PKC-dependent autocrine pathway involving a cyclo-oxygenase product and a yet-to-be-identified myocardial prostanoid receptor.

scholarly journals Role of prostaglandin-mediated cyclic AMP formation in protein kinase C-dependent secretion of atrial natriuretic peptide in rat cardiomyocytes

1994 ◽  
Vol 303 (1) ◽  
pp. 217-225 ◽  
Author(s):  
D J Church ◽  
V Van der Bent ◽  
M B Vallotton ◽  
U Lang
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cyclic Amp ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Rat Cardiomyocytes ◽  
Endogenous Prostaglandin ◽  
Kinase C ◽  
Camp Formation

The role of endogenous prostaglandin production in phorbol diester-induced myocardial atrial natriuretic peptide (ANP) secretion was investigated in cultured spontaneously beating ventricular rat cardiomyocytes. Incubation of cells with 4 beta-phorbol 12-myristate 13-acetate (PMA; 0.1 microM) led to a rapid response in ANP release, a response accompanied by increases in cellular prostacyclin (PGI2) production, cyclic AMP (cAMP) formation and spontaneous contraction frequency. Although PMA-induced ANP secretion exhibited the pharmacological profile of a protein kinase C (PKC)-mediated event, the response was abolished in the presence of the cyclo-oxygenase inhibitors indomethacin (10 microM) and diclofenac (1 microM), indicating that endogenous prostaglandin production is responsible for PMA-induced ANP secretion in this system. Confirming this, PMA-induced ANP secretion was strongly correlated with endogenous formation of 6-oxo-prostaglandin F1 alpha (r = 0.93, P < 0.0005, n = 11), and exogenously applied PGI2, prostaglandin E2 (PGE2) or prostaglandin F2 alpha (PGF2 alpha) elicited simultaneous increases in cAMP formation, contraction frequency and ANP secretion in these cells. Furthermore, PMA-induced cAMP formation was abolished in the presence of either diclofenac or indomethacin, whereas the cAMP-elevating agent forskolin (0.1 microM) mimicked the secretory and chronotropic effect of PMA in these cells. A role for cAMP in PMA-induced ANP secretion was also apparent insofar as PMA-induced ANP release was substantially decreased in the presence of the Rp-diastereomer of 3′,5′-cyclic adenosine monophosphorothioate (Rp-cAMPS; 10 microM), whereas the cAMP-mimetic agent dibutyryl cAMP (10 microM) provoked a rapid increase in ANP secretion in this system. Finally, the Ca(2+)-channel antagonist nifedipine (0.1 microM) severely decreased PGI2-, PGE2- and PMA-induced ANP secretion without affecting PGF2 alpha-induced peptide release, suggesting that PGI2 and/or PGE2, but not PGF2 alpha, are the prostanoids involved in PMA-induced ANP release. Taken together, these results suggest that PKC activation induces ANP secretion in spontaneously beating rat ventricular cardiomyocytes via an autocrine pathway involving increased PGI2 and/or PGE2 formation, a response leading to the activation of a myocardial adenylate cyclase and, subsequently, to that of a nifedipine-sensitive Ca2+ channel.

Regulation of Atrial Natriuretic Peptide Secretion

Physiology ◽  
1993 ◽  
Vol 8 (6) ◽  
pp. 261-266
Author(s):  
H Ruskoaho ◽  
O Vuolteenaho
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Ventricular Myocytes ◽  
Major Determinant ◽  
Cyclic Monophosphate ◽  
Kinase C ◽  
Peptide Secretion ◽  
Atrial Natriuretic

The major determinant of atrial natriuretic peptide (ANP) secretion is myocyte stretch. Other stimuli, affecting the activity of protein kinase C and the intracellular concentrations of Ca2+ and adenosine 3′, 5′-cyclic monophosphate, can act as secretagogues. Evidence that ANP released from ventricular myocytes contributes to plasma ANP levels is also reviewed.

scholarly journals Sibjotang Increases Atrial Natriuretic Peptide Secretion in Beating Rabbit Atria

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Oh Jeong Kwon ◽  
Hyun Cheol Oh ◽  
Yun Jung Lee ◽  
Hye Yoom Kim ◽  
Rui Tan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Body Fluid ◽  
The Body ◽  
Kinase C ◽  
Blood Pressure Homeostasis ◽  
Atrial Natriuretic

Sibjotang (Shizaotang), traditional herbal medicine formula, which was first documented in the Shanghanlun, has long been prescribed for the treatment of impairment of the body fluid homeostasis. The purpose of the present study was to identify the effects of Sibjotang on the secretion of a cardiac hormone, atrial natriuretic peptide (ANP), one of the main hormones involved in the regulation of the body fluid and blood pressure homeostasis. Water extract of Sibjotang increased ANP secretion concomitantly with an increase in atrial dynamics in a concentration-dependent manner. Sibjotang-induced increase in ANP secretion and positive inotropic effect were attenuated by GO6976 and LY333531, selective inhibitors of conventional protein kinase C, but not Rottlerin, an inhibitor of novelPKCδ. Similarly to the effect of Sibjotang, extracts of components of Sibjotang,Euphorbia kansui, andDaphne genkwa, but notEuphorbia pekinensisandZiziphus jujuba, increased ANP secretion and atrial dynamics. Ingredients of Sibjotang, apigenin, rosmarinic acid, and salvianolic acid B decreased ANP secretion and atrial dynamics. These findings suggest that Sibjotang increases ANP secretion and atrial dynamics via activation of conventional protein kinase C signaling. This finding provides experimental evidence for the rationale in the use of Sibjotang in the treatment of impairment of the regulation of body fluid and blood pressure homeostasis.

scholarly journals Effect of Luminal Atrial Natriuretic Peptide on Chloride Reabsorption in Mouse Cortical Thick Ascending Limb

2000 ◽  
Vol 11 (10) ◽  
pp. 1791-1797
Author(s):  
CLAIRE BAILLY
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Specific Inhibitor ◽  
Guanosine Monophosphate ◽  
Thick Ascending Limb ◽  
Kinase C ◽  
Atrial Natriuretic

Abstract. Insofar as neutral endopeptidase inhibition has afforded evidence for a tubular luminal action of atrial natriuretic peptide (ANP), the present study was undertaken to investigate a possible effect of the peptide on chloride reabsorption (JCl) in thick ascending limb (TAL). Luminal addition of ANP to in vitro microperfused cortical TAL (CTAL) significantly decreased JCl with a threshold and a maximum concentration of 10-12 M and 10-9 M, respectively. A similar effect of 10-9 M ANP was observed in medullary TAL (MTAL). The effect of luminal ANP was significantly reduced by HS-142-1, a specific inhibitor of guanylyl cyclase receptor, and by H-8, a protein kinase G inhibitor, but was not affected by the protein kinase C inhibitor bisindolylmaleimide I. Unexpectedly, the effect of ANP was not additive with that of endothelin (ET), a peptide that was previously shown to decrease JCl in TAL through a calcium-independent, protein kinase C—mediated pathway. Indeed, ET-1 (10-8 M in the lumen) significantly decreased JCl and prevented a further effect of ANP on the same tubule. Similarly, the decrease of JCl induced by simultaneous addition of ET and ANP was not higher than that obtained with each agent alone. Conversely, the inhibitory effect of ANP was enhanced in the presence of cyclic guanosine monophosphate (cGMP; 10-6 M in the lumen). ET-1 significantly attenuated the ANP-stimulated generation of cGMP in microdissected CTAL and failed to prevent a further decrease of JCl promoted by a permeant cGMP analogue. It is concluded that luminal ANP decreased Cl reabsorption in mouse CTAL and MTAL. This effect was abrogated by ET-1 as a result of the inhibition of ANP-stimulated cGMP generation.

Inhibition of epithelial Na+ transport by atriopeptin, protein kinase c, and pertussis toxin

1987 ◽  
Vol 253 (2) ◽  
pp. F372-F376 ◽  
Author(s):  
M. Mohrmann ◽  
H. F. Cantiello ◽  
D. A. Ausiello
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Regulatory Protein ◽  
Guanine Nucleotide ◽  
Kinase C ◽  
Guanine Nucleotide Regulatory Protein ◽  
Na Uptake ◽  
Atrial Natriuretic

We have recently shown the selective inhibition of an amiloride-sensitive, conductive pathway for Na+ by atrial natriuretic peptide and 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) in the renal epithelial cell line, LLC-PK1. Using 22Na+ fluxes, we further investigated the modulation of Na+ transport by atrial natriuretic peptide and by agents that increase cGMP production, activate protein kinase c, or modulate guanine nucleotide regulatory protein function. Sodium nitroprusside increases intracellular cGMP concentrations without affecting cAMP concentrations and completely inhibits amiloride-sensitive Na+ uptake in a time- and concentration-dependent manner. In contrast, 8-BrcAMP is without effect on Na+ uptake through the Na+ channel. 1-Oleoyl 2-acetylglycerol (10 micrograms/ml) and phorbol 12-myristate 13-acetate (100 nM), activators of protein kinase c, inhibit Na+ uptake by 93 +/- 13 and 51 +/- 10%, respectively. Prolonged incubation with phorbol ester results in the downregulation of protein kinase c activity and reduces the inhibitory effect of atrial natriuretic peptide, suggesting that the action of this peptide involves stimulation of protein kinase c. Pertussis toxin, which induces the ADP-ribosylation of a 41-kDa guanine nucleotide regulatory protein in LLC-PK1 cells, inhibits 22Na+ influx to the same extent as amiloride. Thus, increasing cGMP, activating protein kinase c, and ADP-ribosylating a guanine nucleotide regulatory protein all inhibit Na+ uptake. These events may be sequentially involved in the action of atrial natriuretic peptide.

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