Enhanced hypertrophy in ob/ob mice due to an impairment in expression of atrial natriuretic peptide

Mascareno, Eduardo; Beckles, Daniel L.; Dhar-Mascareño, Manya; Siddiqui, M.A.Q.

doi:10.1016/j.vph.2009.06.005

Cited by 22 publications

(13 citation statements)

References 37 publications

(45 reference statements)

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“…However, Mascareno et al (64) reported that leptin has antihypertrophic action in vivo in mice, rather than a hyperthrophic effect, as expected by the studies in the culture of ventricular cardiomyocytes. This effect is indeed mediated in vivo by CNHs, since leptin was found to increase the expression of the ANP gene by the activation of nuclear factor of activated T-cell domain of ANP gene promoter (64). On the contrary, Yuan et al (107) reported that intravenous infusion of leptin reduces ANP plasma levels via an NOdependent mechanism in rats.…”

Section: The Cross Talk Between the Cardiac Endocrine Function And Admentioning

confidence: 69%

“…1 and Table 1). Furthermore, several studies reported that arginine vasopressin (97), glucocorticoids (21,64,65), thyroid hormones (4,33), female sex steroids (15,60), some growth factors (27,39), and some cytokines (e.g., TNF-␣, interleukin-1, and interleukin-6) (19,60,90) stimulate CNH production/secretion (Table 1). On the contrary, nitric oxide (NO) exerts a direct inhibitory effect on the production/secretion of CNHs (37,48,107) (Table 1) and also counteracts their relaxant action on cardiac vessels by desensitizing the big conductance calcium-activated potassium channels of vascular smooth muscle (56).…”

Section: The Regulation Of Gene Expression and Production/secretion Omentioning

confidence: 99%

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Thirty years of the heart as an endocrine organ: physiological role and clinical utility of cardiac natriuretic hormones

Clerico

Giannoni

Vittorini

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

173

217

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Clerico A, Giannoni A, Vittorini S, Passino C. Thirty years of the heart as an endocrine organ: physiological role and clinical utility of cardiac natriuretic hormones. Am J Physiol Heart Circ Physiol 301: H12-H20, 2011. First published May 6, 2011; doi:10.1152/ajpheart.00226.2011 reported that atrial extracts contain some biologically active peptides, which promote a rapid and massive diuresis and natriuresis when injected in rats. It is now clear that the heart also exerts an endocrine function and in this way plays a key role in the regulation of cardiovascular and renal systems. The aim of this review is to discuss some recent insights and still-debated findings regarding the cardiac natriuretic hormones (CNHs) produced and secreted by cardiomyocytes (i.e., atrial natriuretic peptide and B-type natriuretic peptide). The functional status of the CNH system depends not only on the production/secretion of CNHs by cardiomyocytes but also on both the peripheral activation of circulating inactive precursor of natriuretic hormones and the transduction of the hormone signal by specific receptors. In this review, we will discuss the data supporting the hypothesis that the production and secretion of CNHs is the result of a complex integration among mechanical, chemical, hemodynamic, humoral, ischemic, and inflammatory inputs. The cross talk among endocrine function, adipose tissue, and sex steroid hormones will be discussed more in detail, considering the clinically relevant relationships linking together cardiovascular risk, sex, and body fat development and distribution. Finally, we will review the pathophysiological role and the clinical relevance of both peripheral maturation of the precursor of B-type natriuretic peptides and hormone signal transduction.B-type natriuretic peptide; sex steroids; adipokines; heart failure; cardiovascular risk THIRTY YEARS AGO, De Bold et al. (20) reported that atrial extracts contain some biological active peptides, which promote a rapid and massive diuresis and natriuresis when injected in rats. Several endogenous peptide hormones with natriuretic and vasodilator activity have been identified in the human blood and peripheral tissues (3,30,69,85,86). Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and their related peptides are predominantly produced by atrial and ventricular cardiomyocytes. The term "cardiac natriuretic hormones" (CNHs) will be used in this review to indicate these two families of natriuretic peptides. Another natriuretic peptide, named C-type natriuretic peptide (CNP), is predominantly produced by the endothelial cells, including those of cardiac vessels. Finally, urodilatin is an NH 2 -terminal (NT) 4-amino acid (aa) extented form of ANP, which is produced by the same ANP gene and secreted into the urine by renal tubular cells (16,34,69).From the original observations made 30 years ago, the advances in this particular research field have determined a complete revision about the role of the heart. It is now clear that the heart also exerts a...

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Section: The Cross Talk Between the Cardiac Endocrine Function And Admentioning

confidence: 69%

Section: The Regulation Of Gene Expression and Production/secretion Omentioning

confidence: 99%

Thirty years of the heart as an endocrine organ: physiological role and clinical utility of cardiac natriuretic hormones

Clerico

Giannoni

Vittorini

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

173

217

View full text Add to dashboard Cite

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“…ANP is released mainly from atrial myocytes into the bloodstream in response to stretch (10,13,22), causing diuresis, natriuresis, and vasodilation (7). Impairment of ANP release or change in its biological receptors causes hypertension or cardiac hypertrophy (20,25). A recent study has suggested an influence of leptin on ANP secretion (20).…”

mentioning

confidence: 99%

“…Impairment of ANP release or change in its biological receptors causes hypertension or cardiac hypertrophy (20,25). A recent study has suggested an influence of leptin on ANP secretion (20). Thus, ob/ob leptin-deficient mice with transverse aortic constriction enhanced cardiac hypertrophy and blunted an increased ANP gene in the ventricle (20).…”

mentioning

confidence: 99%

Leptin reduces plasma ANP level via nitric oxide-dependent mechanism

Yuan¹,

Shah³

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Leptin is a circulating adipocyte-derived hormone that influences blood pressure (BP) and metabolism. This study was designed to define the possible role of leptin in regulation of the atrial natriuretic peptide (ANP) system using acute and chronic experiments. Intravenous infusion of rat leptin (250 g/kg injection plus 2 g·kg Ϫ1 ·min Ϫ1 for 20 min) into Sprague-Dawley rats increased BP by 25 mmHg and decreased plasma level of ANP from 80.3 Ϯ 3.45 to 51.8 Ϯ 3.3 pg/ml. Reserpinization attenuated the rise in BP, but not the reduction of plasma ANP during leptin infusion. N -nitro-L-arginine methyl ester prevented the effects of leptin on the reduction of ANP level. In hyperleptinemic rats that received adenovirus containing rat leptin cDNA (AdCMV-leptin), BP increased during first 2 days and then recovered to control value. Plasma concentration of ANP and expression of ANP mRNA, but not of atrial ANP, in hyperleptinemic rats were lower than in the control groups on the first and second week after administration of AdCMV-leptin. These effects were not observed by the pretreatment with N -nitro-L-arginine methyl ester. No differences in renal function and ANP receptor density in the kidney were found between hyperleptinemic and control rats. Basal ANP secretion and isoproterenol-induced suppression of ANP secretion from isolated, perfused atria of hyperleptinemic rats were not different from those of other control groups. These data suggest that leptin inhibits ANP secretion indirectly through nitric oxide without changing basal or isoproterenolinduced ANP secretion. sympathetic nervous system; atrial natriuretic peptide; adenosine 3=,5=-cyclic monophosphate; hypertension; receptor LEPTIN IS A CIRCULATING adipocyte-derived hormone that regulates energy balance through binding to leptin receptors (Ob-R) at the hypothalamus (37). Leptin decreases appetite and increases body temperature and energy consumption, thereby decreasing adipose tissue mass and body weight (BW) (11,28,32). The Ob-R is a member of the extended class I cytokine receptor family, with at least six splice variants, Ob-R (a-f) (27), and is distributed in various tissues, such as lung, kidney, heart, vascular endothelium, and brain (23, 31). Wide distributions of the Ob-R and leptin mRNA suggest a diversity of its functions. In addition to the well-known metabolic functions of leptin, it also regulates autonomic, cardiovascular, endocrine, and renal functions. However, these functions are still controversial and are under investigation (22). Recent studies have focused on the potential effects of leptin on blood pressure (BP) and renal function through activation of the sympathetic nervous system (SNS). Dose-dependent increases in sympathetic discharge from the kidney and brown adipose tissue by murine leptin have been reported (15). Acute intravenous infusion of leptin showed no effect on BP (15, 16), whereas chronic infusion of murine leptin caused an increase in BP and heart rate (HR), as well as renal vascular resistance (6). Hypertension was deve...

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“…To our knowledge, our study is the fi rst to implicate leptin in the pathogenesis of CSA and also the fi rst to demonstrate a potentially inhibitory interaction between leptin and NPs in patients with HF and CSA. This apparent counterregulatory relationship 22,23,30,31 may account for previous reports of low NP levels in obese patients with HF. 32 Our observation that leptin concentration in patients with HF and CSA is low may be attributable to the presence of high ANP and BNP levels and is consistent with in vitro 22,23 and rodent studies 31,33 that have shown that ANP decreases leptin release from adipocytes.…”

Section: Discussionmentioning

confidence: 65%