Differential regulation of cardiac ANP and BNP mRNA  in different stages of experimental heart failure

Langenickel, Thomas; Pagel, Ines; Höhnel, Klaus; Dietz, Rainer; Willenbrock, Roland

doi:10.1152/ajpheart.2000.278.5.h1500

Cited by 95 publications

(75 citation statements)

References 43 publications

(48 reference statements)

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“…Our data indicate that changes occur in the expression of these genes, and that these changes are coincident with the onset and progression of the structural and metabolic changes seen in the db/db group. The recapitulation of the fetal gene program (i.e., an MHC isoform switch from predominantly ␣ to ␤, decreased SERCA2a, and increased ANP) classically occurs to varying extents in response to a number of mechanical insults, including thoracic aortic constriction (15,34), pacing-induced heart failure (52), and aortocaval shunting (37). However, there is a growing body of evidence that certain metabolic disturbances, including hypothyroidism (24), dexamethasone treatment (21), gonadectomy (57), and a high-cholesterol diet (32), produce these changes as well.…”

Section: Discussionmentioning

confidence: 99%

Magnetic resonance imaging of progressive cardiomyopathic changes in the db/db mouse

Yue

Arai²,

Terashima³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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The db/db mouse is a well-established model of diabetes. Previous reports have documented contractile dysfunction (i.e., cardiomyopathy) in these animals, although the extant literature provides limited insights into cardiac structure and function as they change over time. To better elucidate the natural history of cardiomyopathy in db/db mice, we performed cardiac magnetic resonance (CMR) scans on these animals. CMR imaging was conducted with a 4.7-T magnet on female db/db mice and control db/ϩ littermates at 5, 9, 13, 17, and 22 wk of age. Gated gradient echo sequences were used to obtain cineographic short-axis slices from apex to base. From these images left ventricular (LV) mass (LVM), wall thickness, end-diastolic volume (LVEDV), and ejection fraction (LVEF) were determined. 18 F]FDG metabolic imaging showed a 40% decrease in glucose uptake in db/db mice. Furthermore, contractile dysfunction was observed in 15-wk db/db mice undergoing pressure-volume loops. Finally, real-time quantitative PCR revealed an age-dependent recapitulation of the fetal gene program, consistent with a myopathic process. In summary, as assessed by CMR, db/db mice develop characteristic structural and functional changes consistent with cardiomyopathy. diabetes mellitus; insulin resistance; heart failure; metabolism CONGESTIVE HEART FAILURE (CHF) is a significant yet often underappreciated complication of diabetes mellitus (25). While atherosclerotic coronary artery disease is highly prevalent and likely responsible for CHF in many diabetic patients, findings from several large-scale heart failure clinical trials reveal a 16 -20% prevalence of diabetes in patients with nonischemic cardiomyopathy (9). Moreover, an analysis of hospital discharge data showed a 27% prevalence of diabetes in patients discharged with idiopathic cardiomyopathy, compared with 18% for control subjects (13). Collectively these data suggest an alternative mechanism for CHF in diabetics-one independent of the effects of epicardial coronary disease. However, studies investigating this unique form of "diabetic cardiomyopathy" (51) have failed to establish a unifying mechanistic basis for this phenomenon.The C57BL/KLS-lepr db /lepr db (db/db) mouse, which has a mutation in the leptin receptor, is a well-established animal model of Type 2 diabetes mellitus (19). Leptin resistance results in hyperphagia and weight gain from birth. Homozygous db/db mice become noticeably obese by 3-4 wk of age and develop hyperglycemia at 4 -8 wk. Serum insulin levels increase as early as 10 -14 days, peak at 6 -8 wk, then decrease precipitously afterward (although db/db mice continue to be hyperinsulinemic throughout life). This drop, which is believed to be secondary to pancreatic islet cell dysfunction, further exacerbates the hyperglycemia.In addition to these characteristic phenotypic changes, db/db mice also develop cardiomyopathy. Metabolic experiments using cultured db/db cardiomyocytes have shown impaired glucose oxidation as early as 6 wk of age (1). Echocardiographic studie...

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Section: Discussionmentioning

confidence: 99%

Magnetic resonance imaging of progressive cardiomyopathic changes in the db/db mouse

Yue

Arai²,

Terashima³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…Their findings suggest that ANP and BNP share a common regulatory mechanism and that their synthesis may be commonly associated with atrial stretch. Indeed, wall stretch is known to be an important factor in the induction of ANP and BNP genes in cardiac tissue in CHF (Yasue et al 1994;Magga et al 1997, Langenickel et al 2000.…”

Section: Discussionmentioning

confidence: 99%

“…BNP is considered to be a more reliable prognostic marker than ANP in patients with CHF (Friedl et al 1999), and BNP levels found in the atrium are proportionally related to the severity of the disease (Mukoyama et al 1991;Langenickel et al 2000). Doyama et al (1998) observed that BNP levels rise in response to increased atrial pressure and that atrial expression of BNP mRNA is correlated with that of ANP, assuming that these two genes may share some common regulatory mechanism, of which atrial pressure was suggested to be of major importance.…”

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confidence: 99%

“…At present, there is no conclusive evidence to favor either one of these concepts. Most recently, Langenickel et al (2000) demonstrated that compensated CHF was associated with overexpression of ventricular and atrial ANP but not BNP, whereas in overt heart failure the expression of both ANP and BNP was enhanced. These data suggest that, in contrast to ANP, cardiac BNP expression induced specifically in overt heart failure may be a useful marker for the transition from compensated to overt heart failure.…”

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confidence: 99%

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Evaluation of Atrial Natriuretic Peptide and Brain Natriuretic Peptide in Atrial Granules of Rats with Experimental Congestive Heart Failure

Bialik

Abassi²,

Hammel

et al. 2001

J Histochem Cytochem.

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S U M M A R YThe natriuretic peptides are believed to play an important role in the pathophysiology of congestive heart failure (CHF). We utilized a quantitative cytomorphometric method, using double immunocytochemical labeling, to assess the characteristics of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in atrial granules in an experimental model of rats with CHF induced by aortocaval fistula. Rats with CHF were further divided into decompensated (sodium-retaining) and compensated (sodium-excreting) subgroups and compared with a sham-operated control group. A total of 947 granules in myocytes in the right atrium were analyzed, using electron microscopy and a computerized analysis system. Decompensated CHF was associated with alterations in the modal nature of granule content packing, as depicted by moving bin analysis, and in the granule density of both peptides. In control rats, the mean density of gold particles attached to both peptides was 347.0 Ϯ 103.6 and 306.3 Ϯ 89.9 gold particles/ m 2 for ANP and BNP, respectively. Similar mean density was revealed in the compensated rats (390.6 Ϯ 81.0 and 351.3 Ϯ 62.1 gold particles/ m 2 for ANP and BNP, respectively). However, in rats with decompensated CHF, a significant decrease in the mean density of gold particles was observed (141.6 Ϯ 67.3 and 158.0 Ϯ 71.2 gold particles/ m 2 for ANP and BNP, respectively; p Ͻ 0.05 compared with compensated rats, for both ANP and BNP). The ANP:BNP ratio did not differ between groups. These findings indicate that the development of decompensated CHF in rats with aortocaval fistula is associated with a marked decrease in the density of both peptides in atrial granules, as well as in alterations in the quantal nature of granule formation. The data further suggest that both peptides, ANP and BNP, may be regulated in the atrium by a common secretory mechanism in CHF.

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“…Nonetheless, shunt closure has been reported in 7% of the cases, which means that it is necessary to confirm the patency of the shunt at the end of investigation. Of note that, not only the duration, but also the size of the shunt will determine the onset and severity of CHF in rats, with elevation of LV end-diastolic pressure reported only in the overt CHF group caused by a large shunt for a minimum period of 4 weeks [148]. This procedure has the advantage of being fast and usually well tolerated, despite the limitation of requiring a laparotomy.…”

Section: Volume-overload-induced Hfmentioning

confidence: 99%

Rodent models of heart failure: an updated review

et al. 2012

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Heart failure (HF) is one of the major health and economic burdens worldwide, and its prevalence is continuously increasing. The study of HF requires reliable animal models to study the chronic changes and pharmacologic interventions in myocardial structure and function and to follow its progression toward HF. Indeed, during the past 40 years, basic and translational scientists have used small animal models to understand the pathophysiology of HF and find more efficient ways of preventing and managing patients suffering from congestive HF (CHF). Each species and each animal model has advantages and disadvantages, and the choice of one model over another should take them into account for a good experimental design. The aim of this review is to describe and highlight the advantages and drawbacks of some commonly used HF rodents models, including both non-genetically and genetically engineered models, with a specific subchapter concerning diastolic HF models.

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Differential regulation of cardiac ANP and BNP mRNA in different stages of experimental heart failure

Cited by 95 publications

References 43 publications

Magnetic resonance imaging of progressive cardiomyopathic changes in the db/db mouse

Magnetic resonance imaging of progressive cardiomyopathic changes in the db/db mouse

Evaluation of Atrial Natriuretic Peptide and Brain Natriuretic Peptide in Atrial Granules of Rats with Experimental Congestive Heart Failure

Rodent models of heart failure: an updated review

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