Regional appearance of atrial natriuretic peptide in the ventricles of infarcted rat hearts

Larsen, Terje H.; Sætersdal, Thorvald

doi:10.1007/bf02915128

Cited by 16 publications

(15 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In these particular cells, the intensity of ANP immunoreactivity was stronger compared with the bulk of ANP-positive cells in the myocardium. The appearance of ANPpresenting myocytes near fibrotic lesions has been described in other pathological conditions of the heart such as postinfarction, at the lateral border of the scar, adjacent to the noncontracting myocardium (Takemura et al 1990;Larsen and Saetersdal 1993). Similarly, a strong ANP immunoreactivity was detected in myocytes on the border zone and within the fibrous tissue in ventricular aneurysm.…”

Section: Discussionmentioning

confidence: 80%

Occurrence and distribution of atrial natriuretic peptide-containing cells in the left ventricle of hypertensive rats

Kaganovsky

Belkin

Barhum

et al. 2001

Cell and Tissue Research

View full text Add to dashboard Cite

In the ventricles of adult mammalian hearts, production of atrial natriuretic peptide (ANP) is negligible, restricted to the impulse-conducting cells, the papillary muscles, and a minority of subendocardial myocytes. ANP expression is reinduced in the ventricles of pressure-overloaded and failing hearts and is frequently used as a marker for myocyte hypertrophy. Using an immunohistochemical approach, we have characterized the size distribution of ANP-containing myocytes in the left ventricle of the spontaneously hypertensive rat (SHR) before and after chronic antihypertensive therapy and compared the results to age-matched normotensive Wistar rats (WR). Our findings show that in SHR the frequency of cells presenting ANP granularity is positively correlated with myocyte size (r=0.746, P<0.02). The highest proportion of ANP-positive myocytes (55-57%) was measured among cells of diameters 30-34 microm. In any corresponding cell size, the proportion of ANP-presenting myocytes was five- to tenfold higher in SHR than in the normotensive WR. We studied the effects of the antihypertensive drugs captopril, hydralazine, and nifedipine and found that, regardless of their effect on blood pressure or hypertrophy, all three eliminated ANP immunoproducts from the majority of the left ventricular myocytes and reduced the level of ANP mRNA, captopril being the most effective. The positive correlation between myocyte size and ANP expression was not maintained in the hearts of drug-treated SHR. Myocytes on the border of fibrotic areas or in regions of ANP presentation within the normal heart resisted the suppressive effect of the antihypertensive therapy, indicating that blood pressure or hypertrophy are not the sole correlates for ANP expression.

show abstract

Section: Discussionmentioning

confidence: 80%

Occurrence and distribution of atrial natriuretic peptide-containing cells in the left ventricle of hypertensive rats

Kaganovsky

Belkin

Barhum

et al. 2001

Cell and Tissue Research

View full text Add to dashboard Cite

show abstract

“…The same authors reported a 51% increase in ANP concentration in the coronary effluent from the rat isolated heart subjected to 30 min regional ischemia [83]. Rat intact hearts subjected to 1, 2, 3, 4, 6 days, and 3 weeks left coronary artery (LCA) ligation, exhibited differential ANP immunoreactivity [84]. ANP immunoreactivity was restricted to relatively few ventricular myocytes (comprising the conduction system) after 1 day LCA ligation.…”

Section: Natriuretic Peptidesmentioning

confidence: 94%

“…ANP immunoreactivity was restricted to relatively few ventricular myocytes (comprising the conduction system) after 1 day LCA ligation. However, following 2-3 days LCA ligation, ANP immunoreactivity was apparent in viable tissue of the lateral border of the myocardial infarct, and left ventricular subendocardium [84]. Sustained LCA ligation for 3 weeks was associated with marked ANP immunoreactivity across the whole lateral border area of the myocardial infarct [84].…”

Section: Natriuretic Peptidesmentioning

confidence: 96%

Cardioprotective actions of peptide hormones in myocardial ischemia

2007

View full text Add to dashboard Cite

The myocardium represents a major source of several families of peptide hormones under normal physiological conditions and the plasma concentrations of many of these "cardiac peptides" (or related pro-peptide fragments) are substantially augmented in many cardiac disease states. In addition to well-characterised endocrine functions of several of the cardiac peptides, pleiotropic functions within the myocardium and the coronary vasculature represent a significant aspect of their actions in health and disease. Here, we focus specifically on the cardioprotective roles of four major peptide families in myocardial ischemia and reperfusion: adrenomedullin, kinins, natriuretic peptides and the urocortins. The patterns of early release of all these peptides are consistent with roles as autacoid cardioprotective mediators. Clinical and experimental research indicates the early release and upregulation of many of these peptides by acute ischemia and there is a convincing body of evidence showing that exogenously administered adrenomedullin, bradykinin, ANP, BNP, CNP and urocortins are all markedly protective against experimental myocardial ischemia-reperfusion injury through a conserved series of cytoprotective signal transduction pathways. Intriguingly, all the peptides examined so far have the potential to salvage against infarction when administered specifically during early reperfusion. Thus, the myocardial secretion of peptide hormones likely represents an early protective response to ischemia. Further work is required to explore the potential therapeutic manipulation of these peptides in acute coronary syndromes and their promise as biomarkers of acute myocardial ischemia.

show abstract

“…The ANF gene is also inducible in the ventricle under pathological circumstances and after exposure to hypertrophic agents (2)(3)(4), including the ␣ 1 -adrenergic agonist phenylephrine (PE) (5). Thus, significant increases in ANF mRNA are found in the mouse ventricle that is stressed by aortic banding (6), in genetic hypertension (7), and in viable ventricular myocardium following experimental infarction (8). Even though ventricular ANF expression has been considered to be a specific molecular marker of hypertrophy, its role in hypertrophy is unclear.…”

Section: Atrial Natriuretic Factor (Anf)mentioning

confidence: 99%

Extracellular Signal-regulated Protein Kinase Activation Is Required for the Anti-hypertrophic Effect of Atrial Natriuretic Factor in Neonatal Rat Ventricular Myocytes

Silberbach

Gorenc

Hershberger

et al. 1999

Journal of Biological Chemistry

View full text Add to dashboard Cite

Atrial natriuretic factor (ANF) inhibits proliferation in non-myocardial cells and is thought to be anti-hypertrophic in cardiomyocytes. We investigated the possibility that the anti-hypertrophic actions of ANF involved the mitogen-activated protein kinase signal transduction cascade. Cultured neonatal rat ventricular myocytes treated for 48 h with the ␣ 1 -adrenergic agonist phenylephrine (PE) had an 80% increase in cross-sectional area (CSA). ANF alone had no effect but inhibited PE-induced increases in CSA by approximately 50%. The mitogen-activated protein kinase/ERK kinase (MEK) inhibitor PD098059 minimally inhibited PE-induced increases in CSA, but it completely abolished ANF-induced inhibition of PE-induced increases. ANF-induced extracellular signal-regulated protein kinase (ERK) nuclear translocation was also eliminated by PD098059. ANF treatment caused MEK phosphorylation and activation but failed to activate any of the Raf isoforms. ANF induced a rapid increase in ERK phosphorylation and in vitro kinase activity. PE also increased ERK activity, and the combined effect of ANF and PE appeared to be additive. ANF-induced ERK phosphorylation was eliminated by PD098059. ANF induced minimal phosphorylation of JNK or p38, indicating that its effect on ERK was specific. ANF-induced activation of ERK was mimicked by cGMP analogs, suggesting that ANF-induced ERK activation involves the guanylyl cyclase activity of the ANF receptor. These data suggest that there is an important linkage between cGMP signaling and the mitogen-activated protein kinase cascade and that selective ANF activation of ERK is required for the anti-hypertrophic action of ANF. Thus, ANF expression might function as the natural defense of the heart against maladaptive hypertrophy through its ability to activate ERK.

show abstract

Regional appearance of atrial natriuretic peptide in the ventricles of infarcted rat hearts

Cited by 16 publications

References 16 publications

Occurrence and distribution of atrial natriuretic peptide-containing cells in the left ventricle of hypertensive rats

Occurrence and distribution of atrial natriuretic peptide-containing cells in the left ventricle of hypertensive rats

Cardioprotective actions of peptide hormones in myocardial ischemia

Extracellular Signal-regulated Protein Kinase Activation Is Required for the Anti-hypertrophic Effect of Atrial Natriuretic Factor in Neonatal Rat Ventricular Myocytes

Contact Info

Product

Resources

About