scholarly journals Maternal expression of atrial natriuretic peptide and the fetal programming of cardiac hypertrophy

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
David WJ Armstrong ◽  
M Yat Tse ◽  
Philip G Wong ◽  
Stephen C. Pang
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Fetal Programming ◽  
Maternal Expression ◽  
Atrial Natriuretic

Alteration of Atrial Natriuretic Peptide and Brain Natriuretic Peptide Gene Expression Associated with Progression and Regression of Cardiac Hypertrophy in Renovascular Hypertensive Rats

1996 ◽  
Vol 90 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Hideo Kawakami ◽  
Hideki Okayama ◽  
Mareomi Hamada ◽  
Kunio Hiwada
Keyword(s):  
Gene Expression ◽  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Regression Of Cardiac Hypertrophy ◽  
Peptide Gene ◽  
Atrial Natriuretic

1. We assessed the changes of atrial natriuretic peptide and brain natriuretic peptide gene expression associated with progression and regression of cardiac hypertrophy in renovascular hypertensive rats (RHR). 2. Two-kidney, one-clip hypertensive rats (6-week-old male Wistar) were made and studied 6 (RHR-1) and 10 weeks (RHR-2) after the procedure. Regression of cardiac hypertrophy was induced by nephrectomy at 6 weeks after constriction, and the nephrectomized rats were maintained further for 4 weeks (nephrectomized rat: NEP). Sham operation was performed, and the rats were studied after 6 (Sham-1) and 10 weeks (Sham-2). Atrial natriuretic peptide and brain natriuretic peptide gene expression in the left ventricle was analysed by Northern blotting. 3. Plasma atrial natriuretic peptide and brain natriuretic peptide were significantly higher in RHR-1 and RHR-2 than in Sham-1, Sham-2 and NEP. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels in RHR-1 were approximately 7.2-fold and 1.8-fold higher than those in Sham-1, respectively, and the corresponding levels in RHR-2 were 13.0-fold and 2.4-fold higher than those in Sham-2, respectively. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels of NEP were normalized. Levels of atrial natriuretic peptide and brain natriuretic peptide mRNA were well correlated positively with left ventricular weight/body weight ratios. There was a significant positive correlation between the levels of atrial natriuretic peptide and brain natriuretic peptide mRNA (r = 0.86, P<0.01). 4. We conclude that the expression of atrial natriuretic peptide and brain natriuretic peptide genes is regulated in accordance with the degree of myocardial hypertrophy and that the augmented expression of these two natriuretic peptides may play an important role in the maintenance of cardiovascular haemodynamics in renovascular hypertension.

Differential Regulation of Ventricular Adrenomedullin and Atrial Natriuretic Peptide Gene Expression in Pressure and Volume Overload in the Rat

1998 ◽  
Vol 94 (4) ◽  
pp. 359-365 ◽  
Author(s):  
Michael Kaiser ◽  
Ole Kahr ◽  
Yasuyuki Shimada ◽  
Pamela Smith ◽  
Martin Kelly ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Mrna Level ◽  
Mrna Levels ◽  
Post Surgery ◽  
Infarction Heart ◽  
Atrial Natriuretic

1. Adrenomedullin is a recently discovered vasodilating and natriuretic peptide whose physiological and pathophysiological roles remain to be established. Like atrial natiuretic peptide adrenomedullin is expressed in the left ventricle. Ventricular expression of atrial natriuretic peptide is known to be markedly increased by volume or pressure overload. In this study we investigated whether ventricular expression of adrenomedullin is similarly stimulated under such conditions. 2. Ventricular adrenomedullin and atrial natriuretic peptide mRNA levels as well as those of a loading control mRNA (glyceraldehyde-3-phosphate dehydrogenase) were quantified by Northern blot analysis in (a) rats with severe post-infarction heart failure induced by left coronary ligation at 30 days post-surgery and (b) in rats with pressure-related cardiac hypertrophy induced by aortic banding at several time points (0.5, 1 and 4 h, and 1, 4, 7 and 28 days) after surgery. Levels were compared with those in matched sham-operated controls. 3. The mRNA level of atrial natriuretic peptide was markedly increased (8–10-fold) in the left ventricle of animals with post-infarction heart failure. In contrast, there was only a modest (40%) increase in the level of adrenomedullin mRNA. In rats with pressure-induced cardiac hypertrophy the ventricular level of atrial natriuretic peptide mRNA was again markedly increased (maximum 10-fold). The increase was first noticeable at 24 h post-banding and persisted until 28 days. In contrast, there was no change in adrenomedullin mRNA level compared with sham-operated rats at any time point. 4. Despite having similar systemic effects, the expression of adrenomedullin and atrial natriuretic peptide in the left ventricle is differently regulated. The findings imply distinct roles for the two peptides. The results do not support an important role for ventricular adrenomedullin expression in the remodelling process that occurs during the development of cardiac hypertrophy but suggest that ventricular adrenomedullin participates in the local and/or systemic response to heart failure

Atrial natriuretic peptide behaviour and myocyte hypertrophic profile in combined pressure and volume-induced cardiac hypertrophy

2007 ◽  
Vol 25 (9) ◽  
pp. 1940-1950 ◽  
Author(s):  
Susana Cavallero ◽  
Germ??n E Gonz??lez ◽  
Ana M Puy?? ◽  
Mar??a I Ros??n ◽  
Susana P??rez ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Atrial Natriuretic

Significance of ERK cascade compared with JAK/STAT and PI3-K pathway in gp130-mediated cardiac hypertrophy

2000 ◽  
Vol 279 (4) ◽  
pp. H1635-H1644 ◽  
Author(s):  
Hiroaki Kodama ◽  
Keiichi Fukuda ◽  
Jing Pan ◽  
Motoaki Sano ◽  
Toshiyuki Takahashi ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Janus Kinase ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Extracellular Signal ◽  
Atrial Natriuretic

We compared the role of the Raf-1/mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MEK)/extracellular signal-regulated protein kinase (ERK)/p90RSK cascade in gp130-mediated cardiac hypertrophy with the contribution of the Janus kinase (JAK)/signal transduction and activation of transcription (STAT) and phosphatidylinositide 3-kinase (PI3-K) pathways. Primary cultured neonatal rat cardiomyocytes were stimulated with leukemia inhibitory factor (LIF). LIF sequentially activated Raf-1, MEK1/2, ERK1/2, and p90RSK. We used PD-98059 (a specific MEK inhibitor), AG-490 (a JAK2 inhibitor), and wortmannin (a PI3-K inhibitor) to confirm that this cascade was independent of the JAK/STAT and PI3-K/p70 S6 kinase (S6K) pathways. PD-98059, AG-490, and wortmannin suppressed the LIF-induced increase in [3H]phenylalanine uptake by 54.7, 21.5, and 25.6%, respectively, and inhibited the increase in cell area by 61.2, 42.8, and 39.2%, respectively. Reorganization of myofilaments was predominantly suppressed by AG-490. LIF-induced expression of c- fos, brain natriuretic peptide, and skeletal α-actin mRNA was markedly suppressed by PD-98059 and moderately suppressed by wortmannin and AG-490. Atrial natriuretic peptide was significantly suppressed by AG-490. These findings indicate that this pathway is critically involved in protein synthesis, induction of c- fos, brain natriuretic peptide, and skeletal α-actin expression and is partially involved in myofilament reorganization and atrial natriuretic peptide induction in gp130-mediated cardiac hypertrophy.

Molecular characterisation of neonatal cardiac hypertrophy and its regression

2004 ◽  
Vol 14 (5) ◽  
pp. 498-505 ◽  
Author(s):  
Bamini Gopinath ◽  
Ronald J. Trent ◽  
Bing Yu
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Myosin Heavy Chain ◽  
Natriuretic Peptide ◽  
Heavy Chain ◽  
Maternal Diabetes ◽  
New Drugs ◽  
Complete Regression ◽  
Significant Difference ◽  
Atrial Natriuretic

Neonatal cardiac hypertrophy associated with diabetic pregnancy is transient and regresses naturally, but is associated with increased morbidity and mortality.This study was undertaken to analyse the changes in expression of 5 cardiac genes, including atrial natriuretic peptide, α- and β-myosin heavy chain, and cardiac and skeletal α-actin genes, using a rat neonatal model, in which cardiac hypertrophy was induced via maternal diabetes.In the hypertrophied left ventricle of neonates from diabetic mothers, the levels of mRNA from all the above genes except skeletal α-actin were increased by between 1.8- and 12-fold compared with the controls at birth (p < 0.05). In the first 28 days, the level of mRNA for α-myosin heavy chain increased slightly, while that for atrial natriuretic peptide and β-myosin heavy chain decreased continuously similar to the controls, but at a significantly faster rate. No significant difference between the two groups of neonates was observed in all 5 genes after 1 month, indicating complete regression.Expression of 5 cardiac genes in the neonatal cardiac hypertrophy was characterised in both hypertrophic and regressive phases. Hypertrophic regression provides a unique model for the testing of new drugs or genetic modifying factors in cardiac hypertrophy.

scholarly journals Deficiency of Cardiac Natriuretic Peptide Signaling Promotes Peripartum Cardiomyopathy-Like Remodeling in the Mouse Heart

Circulation ◽  
2020 ◽  
Vol 141 (7) ◽  
pp. 571-588 ◽  
Author(s):  
Kentaro Otani ◽  
Takeshi Tokudome ◽  
Chizuko A. Kamiya ◽  
Yuanjie Mao ◽  
Hirohito Nishimura ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Knockout Mice ◽  
Interleukin 6 ◽  
Perinatal Period ◽  
Lactation Period ◽  
Wild Type ◽  
Atrial Natriuretic

Background: The maternal circulatory system and hormone balance both change dynamically during pregnancy, delivery, and the postpartum period. Although atrial natriuretic peptides and brain natriuretic peptides produced in the heart control circulatory homeostasis through their common receptor, NPR1, the physiologic and pathophysiologic roles of endogenous atrial natriuretic peptide/brain natriuretic peptide in the perinatal period are not fully understood. Methods: To clarify the physiologic and pathophysiologic roles of the endogenous atrial natriuretic peptide/brain natriuretic peptide–NPR1 system during the perinatal period, the phenotype of female wild-type and conventional or tissue-specific Npr1-knockout mice during the perinatal period was examined, especially focusing on maternal heart weight, blood pressure, and cardiac function. Results: In wild-type mice, lactation but not pregnancy induced reversible cardiac hypertrophy accompanied by increases in fetal cardiac gene mRNAs and ERK1/2 (extracellular signaling-regulated kinase) phosphorylation. Npr1-knockout mice exhibited significantly higher plasma aldosterone level than did wild-type mice, severe cardiac hypertrophy accompanied by fibrosis, and left ventricular dysfunction in the lactation period. Npr1-knockout mice showed a high mortality rate over consecutive pregnancy–lactation cycles. In the hearts of Npr1-knockout mice during or after the lactation period, an increase in interleukin-6 mRNA expression, phosphorylation of signal transducer and activator of transcription 3, and activation of the calcineurin–nuclear factor of the activated T cells pathway were observed. Pharmacologic inhibition of the mineralocorticoid receptor or neuron-specific deletion of the mineralocorticoid receptor gene significantly ameliorated cardiac hypertrophy in lactating Npr1-knockout mice. Anti–interleukin-6 receptor antibody administration tended to reduce cardiac hypertrophy in lactating Npr1-knockout mice. Conclusions: These results suggest that the characteristics of lactation-induced cardiac hypertrophy in wild-type mice are different from exercise-induced cardiac hypertrophy, and that the endogenous atrial natriuretic peptide/brain natriuretic peptide–NPR1 system plays an important role in protecting the maternal heart from interleukin-6–induced inflammation and remodeling in the lactation period, a condition mimicking peripartum cardiomyopathy.

Sign in / Sign up

Export Citation Format

Share Document