The heart is the center of a new endocrine, paracrine, and neuroendocrine system.

Forssmann, Wolf‐Georg; Nokihara, Kiyoshi; Gagelmann, M.; Hock, D.; Feller, Stephan M.; Schulz‐Knappe, Peter; Herbst, F.

doi:10.1679/aohc.52.suppl_293

Cited by 47 publications

(23 citation statements)

References 81 publications

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“…AVP does not seem to participate in this water and sodium homeostasis either, since the plasma AVP concentrations are not changed after a salt-loading treatment during pregnancy in the rat (5). Urodilatin is a peptide that belongs to the family of natriuretic peptides, located in the distal tubular cells and acting as a paracrine hormone within the kidney (39,40). According to Bub et al (23), urodilatin is stimulated by dietary salt loading and might be involved in the regulation of water and electrolyte balance in the rat.…”

Section: European Journal Of Endocrinology (2000) 142mentioning

confidence: 99%

Atrial natriuretic peptide and aldosterone secretions, and atrial natriuretic peptide-binding sites in kidneys and adrenal glands of pregnant and fetal rats in late gestation in response to a high-salt diet

Deloof

Seze

Montel

et al. 2000

European Journal of Endocrinology

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Objective: This study aimed at determining, in the term pregnant rat, whether maternal and fetal plasma atrial natriuretic peptide (ANP) concentrations were modified in response to an oral sodium load, and to investigate whether any changes in plasma concentrations were able to modify the density and affinity of the different ANP-binding site subtypes in maternal and fetal kidneys and adrenal glands. Methods: Pregnant rats kept in metabolic cages were divided into two groups. The normal sodium diet group had free access to rat chow and tap water whereas the high sodium diet group received 1% NaCl as drinking water for 10 consecutive days from day 11 to day 21 of gestation with free access to standard rat chow. Pregnant rats from both groups were killed by decapitation on day 21 of gestation. The plasma ANP and aldosterone concentrations were determined by RIA. The density and affinity of ANP receptors were determined in the maternal and fetal adrenal glands and kidneys. Results: In the pregnant rats on the high-salt diet, the sodium and water intakes, as well as the urine volume and sodium excretion, were significantly higher than in the control group. After 10 days of high-salt intake, water and sodium retentions were not significantly different in the two groups, indicating that the pregnant rats were able to excrete excess salt. The high sodium intake did not change the body weight of the pregnant rats but did increase the body weight of the fetal rats. Maternal and fetal hematocrits remained unchanged in both groups, the high sodium intake did not modify plasma sodium concentration in the maternal rats but increased that of the fetuses, indicating an accumulation of sodium in the fetal rats. The dietary sodium intake did not change the plasma ANP concentrations but significantly decreased the plasma aldosterone concentrations in both the maternal and fetal rats. In response to the high-salt diet, the density and affinity of total ANP, ANPb and ANPc receptors were not altered in the maternal isolated renal glomeruli or the adrenal zona glomerulosa membranes or the fetal adrenal gland and kidney membrane preparations. Conclusion: These results suggest that ANP is not involved in the regulation of water and electrolyte balance in maternal and fetal rats during salt-loaded intake.

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Section: European Journal Of Endocrinology (2000) 142mentioning

confidence: 99%

Atrial natriuretic peptide and aldosterone secretions, and atrial natriuretic peptide-binding sites in kidneys and adrenal glands of pregnant and fetal rats in late gestation in response to a high-salt diet

Deloof

Seze

Montel

et al. 2000

European Journal of Endocrinology

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“…However, accumulating evidence suggests that other organelles, including the endoplasmic reticulum (ER), lysosomes, and Golgi apparatus, are also major points of integration of proapoptotic signaling or damage sensing (10,14). In particular, in the myocardium, the ER participates in maintenance of cellular calcium homeostasis (57) and synthesis of secretory proteins (16) such as atrial natriuretic peptide, brain natriuretic peptide (15), and vascular endothelial growth factor (VEGF) (51). Dysfunction of the ER might thus contribute to the pathogenesis of heart disease.…”

mentioning

confidence: 99%

AMP-Activated Protein Kinase Protects Cardiomyocytes against Hypoxic Injury through Attenuation of Endoplasmic Reticulum Stress

Terai

Hiramoto²,

Masaki³

et al. 2005

Molecular and Cellular Biology

328

253

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Oxygen deprivation leads to the accumulation of misfolded proteins in the endoplasmic reticulum (ER), causing ER stress. Under conditions of ER stress, inhibition of protein synthesis and up-regulation of ER chaperone expression reduce the misfolded proteins in the ER. AMP-activated protein kinase (AMPK) is a key regulatory enzyme involved in energy homeostasis during hypoxia. It has been shown that AMPK activation is associated with inhibition of protein synthesis via phosphorylation of elongation factor 2 (eEF2) in cardiomyocytes. We therefore examined whether AMPK attenuates hypoxia-induced ER stress in neonatal rat cardiomyocytes. We found that hypoxia induced ER stress, as assessed by the expression of CHOP and BiP and cleavage of caspase 12. Knockdown of CHOP or caspase 12 through small interfering RNA (siRNA) resulted in decreased expression of cleaved poly(ADP-ribose) polymerase following exposure to hypoxia. We also found that hypoxia-induced CHOP expression and cleavage of caspase 12 were significantly inhibited by pretreatment with 5-aminoimidazole-4-carboxyamide-1-␤-D-ribofuranoside (AICAR), a pharmacological activator of AMPK. In parallel, adenovirus expressing dominant-negative AMPK significantly attenuated the cardioprotective effects of AICAR. Knockdown of eEF2 phosphorylation using eEF2 kinase siRNA abolished these cardioprotective effects of AICAR. Taken together, these findings demonstrate that activation of AMPK contributes to protection of the heart against hypoxic injury through attenuation of ER stress and that attenuation of protein synthesis via eEF2 inactivation may be the mechanism of cardioprotection by AMPK.

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“…NP administration revealed significant prevention of wound repair in human coronary arterial lesions, suggesting that NP by endothelial growth hormone function could be useful for therapeutic angiogenesis in cases of wound healing. Forssmann et al reviewed heart hormone, cardiodilatin (CDD), and urodilatin as members of the natriuretic peptides family by showing excellent electron microscopic features (170). The present review deals with supplementary reports for the NP family in bone tissue and further biophysiology in the excretion of mineral salts.…”

Section: Resultsmentioning

confidence: 94%

Natriuretic peptides: potential modulators of circulatory, renal, respiratory, digestive, endocrine, and central nerve systems and implications of their role in bone remodeling

et al. 2009

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The heart is the center of a new endocrine, paracrine, and neuroendocrine system.

Cited by 47 publications

References 81 publications

Atrial natriuretic peptide and aldosterone secretions, and atrial natriuretic peptide-binding sites in kidneys and adrenal glands of pregnant and fetal rats in late gestation in response to a high-salt diet

Atrial natriuretic peptide and aldosterone secretions, and atrial natriuretic peptide-binding sites in kidneys and adrenal glands of pregnant and fetal rats in late gestation in response to a high-salt diet

AMP-Activated Protein Kinase Protects Cardiomyocytes against Hypoxic Injury through Attenuation of Endoplasmic Reticulum Stress

Natriuretic peptides: potential modulators of circulatory, renal, respiratory, digestive, endocrine, and central nerve systems and implications of their role in bone remodeling

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