α1- and β-adrenoceptor stimulation differentially activate p38-MAPK and atrial natriuretic peptide production in the perfused amphibian heart

2002 ◽  
Vol 205 (16) ◽  
pp. 2387-2397 ◽  
Author(s):  
Ioanna-Katerina S. Aggeli ◽  
Catherine Gaitanaki ◽  
Antigone Lazou ◽  
Isidoros Beis
Keyword(s):  
Atrial Natriuretic Peptide ◽  
P38 Mapk ◽  
Natriuretic Peptide ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Mapk Activation ◽  
Adrenergic Agents ◽  
Kinase Phosphorylation ◽  
Amphibian Heart ◽  
Atrial Natriuretic

SUMMARY We investigated the activation of p38-MAPK by various adrenergic agents in the perfused Rana ridibunda heart. Phenylephrine (50 μmol l-1) rapidly induced the differential activation of all three mitogen-activated protein kinase (MAPK) subfamilies (ERK, JNKs and p38-MAPK)in this experimental system. Focusing on p38-MAPK response to phenylephrine,we found that the kinase phosphorylation reached maximal values at 30 s,declining thereafter to basal values at 15 min. p38-MAPK activation by phenylephrine was verified as exclusively α1-AR-mediated. Furthermore, SB203580 (1 μmol l-1) abolished the kinase phosphorylation by phenylephrine. Isoproterenol (50 μmol l-1)was also shown to activate p38-MAPK in a time- and temperature-dependent manner. A marked, sustained p38-MAPK activation profile was observed at 25°C, while at 18°C the kinase response to isoproterenol was modest. Isoproterenol effect on p38-MAPK stimulation was β-AR-mediated. Immunohistochemical studies revealed the enhanced presence of phosphorylated p38-MAPK and atrial natriuretic peptide (ANP) in both phenylephrine- and isoproterenol-stimulated hearts, a reaction completely blocked by the respective specific antagonists, or the specific p38-MAPK inhibitor SB203580. These findings indicate a functional correlation between p38-MAPK activation and ANP accumulation in the perfused amphibian heart.

scholarly journals Atrial Natriuretic Peptide mRNA Regulation by p38- MAPK in the Perfused Amphibian Heart

2005 ◽  
Vol 16 (4-6) ◽  
pp. 183-192 ◽  
Author(s):  
Athanassios Vassilopoulos ◽  
Catherine Gaitanaki ◽  
Panagiota Papazafiri ◽  
Isidoros Beis
Keyword(s):  
Atrial Natriuretic Peptide ◽  
P38 Mapk ◽  
Natriuretic Peptide ◽  
Mrna Regulation ◽  
Amphibian Heart ◽  
Atrial Natriuretic

scholarly journals Atrial Natriuretic Peptide Improves Neurite Outgrowth from Spiral Ganglion Neurons In Vitro through a cGMP-Dependent Manner

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Fei Sun ◽  
Ke Zhou ◽  
Ke-yong Tian ◽  
Jie Wang ◽  
Jian-hua Qiu ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Neurite Outgrowth ◽  
Natriuretic Peptide ◽  
Critical Role ◽  
Spiral Ganglion ◽  
Spiral Ganglion Neurons ◽  
Dependent Manner ◽  
Ganglion Neurons ◽  
Atrial Natriuretic

The spiral ganglion neurons (SGNs) are the primary afferent neurons in the spiral ganglion (SG), while their degeneration or loss would cause sensorineural hearing loss. As a cardiac-derived hormone, atrial natriuretic peptide (ANP) plays a critical role in cardiovascular homeostasis through binding to its functional receptors (NPR-A and NPR-C). ANP and its receptors are widely expressed in the mammalian nervous system where they could be implicated in the regulation of multiple neural functions. Although previous studies have provided direct evidence for the presence of ANP and its functional receptors in the inner ear, their presence within the cochlear SG and their regulatory roles during auditory neurotransmission and development remain largely unknown. Based on our previous findings, we investigated the expression patterns of ANP and its receptors in the cochlear SG and dissociated SGNs and determined the influence of ANP on neurite outgrowth in vitro by using organotypic SG explants and dissociated SGN cultures from postnatal rats. We have demonstrated that ANP and its receptors are expressed in neurons within the cochlear SG of postnatal rat, while ANP may promote neurite outgrowth of SGNs via the NPR-A/cGMP/PKG pathway in a dose-dependent manner. These results indicate that ANP would play a role in normal neuritogenesis of SGN during cochlear development and represents a potential therapeutic candidate to enhance regeneration and regrowth of SGN neurites.

Atrial natriuretic peptide in the eel, Anguilla anguilla L.: its cardiac distribution, receptors and actions on isolated branchial cells

1992 ◽  
Vol 9 (2) ◽  
pp. 103-114 ◽  
Author(s):  
C. L. Broadhead ◽  
U. T. O'Sullivan ◽  
C. F. Deacon ◽  
I. W. Henderson
Keyword(s):  
Sodium Chloride ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Binding Sites ◽  
Specific Binding ◽  
Anguilla Anguilla ◽  
Chloride Cells ◽  
Dependent Manner ◽  
Single Class ◽  
Atrial Natriuretic

ABSTRACT The presence of atrial natriuretic peptide (ANP) and the nature of its binding sites were studied in freshwater (FW)- and seawater (SW)-adapted eels using a heterologous analogue, that of the rat (rANP). Rat ANP-like immunoreactivity was demonstrated in the cardiac atria and ventricles of both FW and SW eels, and electron-dense ANP-like granules were observed. The atria and ventricles of FW eels contained significantly more granules than those of SW animals and, in both types, the atria were more granular than the ventricles. Specific binding sites for rANP were demonstrated by displacement and uptake experiments using labelled rANP in dispersed eel branchial cell preparations, enriched in chloride cells. The concentration of rANP required to produce a 50% inhibition of binding in FW cells was significantly lower than that in SW cells. Scatchard analyses revealed the presence of two classes of binding site in SW eel branchial cells but only a single class of receptor in FW cells. The affinity of the FW receptor was not significantly different from that of the SW high affinity site. Rat ANP stimulated the production of cyclic GMP (cGMP) in a dose-dependent manner, and both basal and stimulated levels of cGMP were significantly greater in SW branchial cells. These studies suggest that ANP is involved in the adaptation of the euryhaline eel to differing environmental salinities; the levels of the peptide in the heart alter with changing salinity, and the nature of the receptors in the sodium chloride-transporting epithelium of the gill changes in response to the need either to eliminate or to absorb sodium chloride.

Endogenous atrial natriuretic peptide inhibits endothelin-1 secretion in dogs with severe congestive heart failure

1996 ◽  
Vol 270 (5) ◽  
pp. H1819-H1824 ◽  
Author(s):  
A. Wada ◽  
T. Tsutamato ◽  
Y. Maeda ◽  
T. Kanamori ◽  
Y. Matsuda ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Severe Congestive Heart Failure ◽  
Dependent Manner ◽  
Endothelin 1 ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) has been shown to counteract the response of endothelin-1 (ET-1), but whether endogenous ANP actually inhibits the systemic release of ET-1 in vivo has not yet been determined. We administered HS-142-1 (HS), a specific antagonist of the guanylate cyclase-coupled ANP receptor, to conscious dogs with severe congestive heart failure (CHF) produced by rapid right ventricular pacing (n = 5, for 22 days) at doses of 0.3, 1.0, and 3.0 mg/kg at 30-minutes intervals. In the present study, plasma ANP and ET-1 levels were significantly elevated in CHF(348 +/-58 and 4.54 +/- 0.60 pg/ml, respectively compared with those in control dogs (65 +/- 4, P < 0.01, 1.30 +/- 0.17 pg/ml, P < 0.001). HS inhibited plasma guanosine 3',5'-cyclic monophosphate (cGMP) levels, a biological market of endogenous ANP activity, in a dose-dependent manner from 21.8 +/- 2.2 to 7.2 +/- 1.4 pmol/ml (P < 0.001), with concomitant significant increases in plasma ET-1 levels from 4.54 +/- 0.60 to 6.60 +/- 0.72 pg/ml (P < 0.05). There was a significant negative correlation between the decrease in plasma cGMP and the increment in plasma ET-1 (r = -0.64, P < 0.01). Despite these responses, mean arterial pressure and pulmonary arterial pressure did not change significantly. Plasma angiotensin II and arginine vasopressin levels, both of which have been reported to stimulate ET-1 secretion in vitro, also showed no significant changes. These results strongly suggest that endogenous ANP directly inhibits endogenous ET-1 secretion through a cGMP-mediated pathway in chronic severe CHF.

scholarly journals Atrial natriuretic peptide attenuates ANG II-induced hypertrophy of renal tubular cells

2001 ◽  
Vol 281 (1) ◽  
pp. F81-F90 ◽  
Author(s):  
Tete Hannken ◽  
Regine Schroeder ◽  
Rolf A. K. Stahl ◽  
Gunter Wolf
Keyword(s):  
Cell Cycle ◽  
Atrial Natriuretic Peptide ◽  
Map Kinase ◽  
Cell Cycle Arrest ◽  
Natriuretic Peptide ◽  
Ang Ii ◽  
Renal Tubular Cells ◽  
Cycle Arrest ◽  
Kinase Phosphorylation ◽  
Atrial Natriuretic

ANG II arrests LLC-PK1 cells in the G1 phase of the cell cycle and induces hypertrophy, an effect mediated by induction of p27Kip1. We studied whether atrial natriuretic peptide (ANP) may modulate ANG II-induced hypertrophy and p27Kip1 expression in tubular LLC-PK1 cells. ANP, through its fragments 3—28and 4—27, prevented ANG II-induced cell cycle arrest. ANP inhibited >80% of ANG II-induced p27Kip1 protein expression (Western blots). ANP stimulated expression of MKP-1, a phosphatase involved in dephosphorylation of p44/42 mitogen-activated protein (MAP) kinase, up to 12 h. ANP prevented the ANG II-mediated phosphorylation peak of MAP kinase after 12 h of stimulation. 8-Bromo-cGMP mimicked all the effects of ANP. Transfection with MKP-1 antisense, but not sense, oligonucleotides abolished the modifying role of ANP on ANG II-mediated cell cycle arrest.. The effect of ANP on ANG II-mediated hypertrophy of LLC-PK1 cells is regulated on the level of MAP kinase phosphorylation, a key step in the induction of p27Kip1. Although ANP and ANG II both stimulate generation of reactive oxygen species, ANP additionally induces expression of MKP-1, leading to interference with ANG II-mediated MAP kinase phosphorylation.

scholarly journals Ethanol Extract ofLepidium apetalumSeed Elicits Contractile Response and Attenuates Atrial Natriuretic Peptide Secretion in Beating Rabbit Atria

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Seung Ju Kim ◽  
Hye Yoom Kim ◽  
Yun Jung Lee ◽  
Hao Zhen Cui ◽  
Ji Yeon Jang ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Pulse Pressure ◽  
Kinase Inhibitor ◽  
Ethanol Extract ◽  
Dependent Manner ◽  
Rabbit Atria ◽  
Volume Pulse ◽  
Atrial Natriuretic

The seeds ofLepidium apetalumWilldenow (called “Tinglizi” in China and “Jungryukza” in Korea) have been used to discharge phlegm and improve dropsy in Oriental medicine. The present study investigated the effects of ethanol extract of the seeds ofLepidium apetalum(ELA) on atrial dynamics and atrial natriuretic peptide (ANP) secretion in beating rabbit atria. ELA increased atrial stroke volume, pulse pressure, and cAMP efflux, concomitantly attenuating ANP secretion in a dose-dependent manner. ELA-induced increases in atrial stroke volume, pulse pressure, and cAMP levels and decrease in ANP secretion were not inhibited by pretreatment with staurosporine, a nonspecific protein kinase inhibitor, or diltiazem and verapamil, the L-type Ca2+channel blockers, respectively. Helveticoside, a well-known digitalis-like cardiac glycosidic constituent of ELA, also increased atrial dynamics, including stroke volume and pulse pressure, without changing cAMP efflux and ANP secretion, and the effects of helveticoside were not inhibited by pretreatment with staurosporine, diltiazem, and verapamil. These results suggest that the ELA-induced positive inotropic activity in beating rabbit atria might, at least partly, be due to the digitalis-like activity of helveticoside rather than an increase in cAMP efflux.

scholarly journals Prolonged Atrial Natriuretic Peptide Exposure Stimulates Guanylyl Cyclase-A Degradation

Endocrinology ◽  
2010 ◽  
Vol 151 (6) ◽  
pp. 2769-2776 ◽  
Author(s):  
Darcy R. Flora ◽  
Lincoln R. Potter
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Guanylyl Cyclase ◽  
Cultured Cells ◽  
Volume Overload ◽  
Receptor Expression ◽  
Dependent Manner ◽  
Down Regulation ◽  
Time Required ◽  
Atrial Natriuretic

Natriuretic peptide receptor-A (NPR-A), also known as guanylyl cyclase-A, is a transmembrane receptor guanylyl cyclase that is activated by the cardiac hormones atrial natriuretic peptide and B-type natriuretic peptide. Although ligand-dependent NPR-A degradation (also known as down-regulation) is widely acknowledged in human and animal models of volume overload, down-regulation in cultured cells is controversial. Here, we examined the effect of ANP exposure on cellular NPR-A levels as a function of time. Relative receptor concentrations were estimated using guanylyl cyclase and immunoblot assays in a wide variety of cell lines that endogenously or exogenously expressed low or high numbers of receptors. ANP exposures of 1 h markedly reduced hormone-dependent but not detergent-dependent guanylyl cyclase activities in membranes from exposed cells. However, 1-h ANP exposures did not significantly reduce NPR-A concentrations in any cell line. In contrast, exposures of greater than 1 h reduced receptor concentrations in a time-dependent manner. The time required for half of the receptors to be degraded (t1/2) in primary bovine aortic endothelial and immortalized HeLa cells was approximately 8 h. In contrast, a 24-h exposure of ANP to 293T cells stably overexpressing NPR-A caused less than half of the receptors to be degraded. To our knowledge, this is the first report to directly measure NPR-A down-regulation in endogenously expressing cells. We conclude that down-regulation is a universal property of NPR-A but is relatively slow and varies with receptor expression levels and cell type.

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