Evidence supporting a physiological role for proANP-(1–30) in the regulation of renal excretion

Dietz, John R.; Scott, D.; Landon, Carol S.; Nazian, Stanley J.

doi:10.1152/ajpregu.2001.280.5.r1510

Cited by 29 publications

(58 citation statements)

References 28 publications

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“…1). The main physiological properties of these four peptide hormones after their release from the heart are blood pressure regulation and the maintenance of plasma volume in animals (Vesely et al 1987, Martin et al 1990, Gunning et al 1992, Benjamin & Peterson 1995, Zeidel 1995, Villarreal et al 1999, Dietz et al 2001 and humans (Vesely et al 1994a(Vesely et al ,b, 1998. The cardiac hormones, synthesized in the atrium of the heart, are long-acting natriuretic peptide (LANP) that consists of the first 30 a.a. from the N-terminal end of the ANP prohormone; vessel dilator, a.a. 31-67; kaliuretic peptide, a.a. 79-98; and ANP, a.a. 99-126 of the 126 a.a. prohormone (Vesely 1992(Vesely , 2002; Fig.…”

Section: Introductionmentioning

confidence: 99%

Cardiac hormones for the treatment of cancer

Vesely¹

2013

Endocrine-Related Cancer

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Four cardiac hormones, namely atrial natriuretic peptide, vessel dilator, kaliuretic peptide, and long-acting natriuretic peptide, reduce up to 97% of all cancer cells in vitro. These four cardiac hormones eliminate up to 86% of human small-cell lung carcinomas, two-thirds of human breast cancers, and up to 80% of human pancreatic adenocarcinomas growing in athymic mice. Their anticancer mechanisms of action, after binding to specific receptors on cancer cells, include targeting the rat sarcoma-bound GTP (RAS) (95% inhibition)-mitogen-activated protein kinase kinase 1/2 (MEK 1/2) (98% inhibition)-extracellular signal-related kinase 1/2 (ERK 1/2) (96% inhibition) cascade in cancer cells. They also inhibit MAPK9, i.e. c-Jun N-terminal kinase 2. They are dual inhibitors of vascular endothelial growth factor (VEGF) and its VEGFR2 receptor (up to 89%). One of the downstream targets of VEGF is b-catenin, which they reduce up to 88%. The WNT pathway is inhibited up to 68% and secreted frizzled-related protein 3 decreased up to 84% by the four cardiac hormones. AKT, a serine/threonine protein kinase, is reduced up to 64% by the cardiac hormones. STAT3, a final 'switch' that activates gene expression that leads to malignancy, is decreased by up to 88% by the cardiac hormones. STAT3 is specifically decreased as they do not affect STAT1. There is a cross-talk between the RAS-MEK 1/2-ERK 1/2 kinase cascade, VEGF, b-catenin, WNT, JNK, and STAT pathways and each of these pathways is inhibited by the cardiac hormones.

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Section: Introductionmentioning

confidence: 99%

Cardiac hormones for the treatment of cancer

Vesely¹

2013

Endocrine-Related Cancer

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“…1). Within the 126 a.a. prohormone in the heart are four peptide hormones whose main biologic properties are blood pressure regulation and maintenance of plasma volume in animals [5][6][7][8][9][10][11] and humans [12][13][14][15][16]. These peptide hormones, numbered by their a.a. sequences beginning at the N-terminal end of the ANP prohormone, consist of the first 30 a.a. of the prohormone-that is, long acting natriuretic peptide (LANP), vessel dilator (a.a. 31-67), kaliuretic peptide (a.a. 79-98), and ANP (a.a. 99-126) [2,3].…”

Section: Cardiac Natriuretic Peptidesmentioning

confidence: 99%

Urodilatin: A better natriuretic peptide?

Vesely

2007

Curr Heart Fail Rep

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The kidney natriuretic peptide urodilatin (ie, ularitide) decreases pulmonary capillary wedge pressure (PCWP) but does not cause diuresis in persons with congestive heart failure (CHF). Thirty-three percent of patients with CHF treated with 30 ng/kg/min ularitide develop hypotension with systolic blood pressures below 90 mmHg. Nesiritide and atrial natriuretic peptide lower PCWP and cause hypotension. They do not produce diuresis or natriuresis in patients with CHF. The best natriuretic peptide for treating CHF is the cardiac hormone vessel dilator which decreases PCWP and decreases systemic and pulmonary vascular resistance while simultaneously increasing cardiac output and cardiac index. What makes the vessel dilator markedly better than atrial natriuretic peptide, nesiritide, and ularitide for treatment of CHF is that it enhances sodium excretion fivefold and causes a fivefold enhanced diuresis in patients with CHF with its biologic effects lasting over 6 hours compared with less than 30 minutes for the above peptides.

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“…Secretion rates calculated from the pro-ANP-(1-30) RIA (3)(4)(5) were used in all NRVM experiments as an index of cardiac hormone secretion. This assay measures the NH 2-terminus of the pro-ANP molecule, and we have shown that in both plasma and in our atrial tissue perfusates the peptide measured by this NH 2-terminal assay is consistent with pro-ANP-(1-30) (3,10).…”

Section: Measurement Of Pro-anp-(1-30) Secretion From Cultured Nrvmmentioning

confidence: 99%

“…The cultured cells were pretreated with the agonists/antagonists for 5 min before exposure to ET-1. Medium was collected at defined incubation times, centrifuged, and assayed for ANP and pro-ANP-(1-30) by RIA using methods previously described by our laboratory (4,5). The data are expressed as picograms of ANP or pro-ANP-(1-30) per tissue culture well or as ANP secretion rate in picograms per minute for atrial perfusates.…”

Section: Measurement Of Pro-anp-(1-30) Secretion From Cultured Nrvmmentioning

confidence: 99%

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CytochromeP-450 metabolites in endothelin-stimulated cardiac hormone secretion

Lee

Landon

Nazian

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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. Cytochrome P-450 metabolites in endothelin-stimulated cardiac hormone secretion. Am J Physiol Regul Integr Comp Physiol 286: R888-R893, 2004. First published January 8, 2004 10.1152/ ajpregu.00482.2003.-We examined the role of cytochrome P-450-arachidonate (CYP450-AA) metabolites in endothelin-1 (ET-1)-stimulated atrial natriuretic peptide (ANP) and pro-ANP-(1-30) secretion from the heart. 17-Octadecynoic acid (17-ODYA, 10 Ϫ5 M) significantly inhibited ANP secretion stimulated by ET-1 (10 Ϫ8 M) in the isolated perfused rat atria and inhibited pro-ANP-(1-30) secretion stimulated by ET-1 (10 Ϫ8 M) or 20-hydroxyeicosatetraenoic acid in cultured neonatal rat ventricular myocytes (NRVM). In NRVM, 17-ODYA significantly (P Ͻ 0.05) increased secretion of cAMP but had no significant effect on the secretion of cGMP from NRVM. Staurosporine, an inhibitor of protein kinase C, completely blocked the inhibitory action of 17-ODYA, whereas a protein kinase A inhibitor, H-89 (5 ϫ 10 Ϫ5 M), did not significantly attenuate the effects of 17-ODYA. The results show that the inhibitory action of 17-ODYA on ET-1-augmented ANP secretion is mediated through cAMP and suggest that CYP450-AA may play an important role in ET-1-induced cardiac hormone secretion.endothelin-1; 20-hydroxyeicosatetraenoic acid; 17-octadecynoic acid; nitric oxide; protein kinase A; protein kinase C; atrial natriuretic peptide; pro-ANP-(1-30); cardiac hypertrophy THE MAMMALIAN HEART SYNTHESIZES and secretes a family of peptides that has potent diuretic, natriuretic, and vascular smooth muscle relaxant effects as well as complex interactions with the hormonal and nervous systems (18,23).Atrial natriuretic peptide (ANP) is secreted by the heart in response to increased atrial stretch (2, 4) such as would typically be produced by an increase in blood volume. ANP is initially stored in granules in the heart as a 126-amino acid prohormone (pro-ANP). During the secretion process (4, 3, 10), the pro-ANP molecule is cleaved to form ANP, the 28-amino acid COOHterminus of pro-ANP, and several NH 2 -terminal prohormone peptides, pro-ANP-(1-30), -(31-67), and -(79-98). Our recent data suggest that pro-ANP-(1-30) also increases sodium excretion and plays a role in blood volume and blood pressure regulation (5).Numerous factors have been shown to modulate the secretion of ANPs, including endothelin-1 (ET-1), a potent vasoconstrictor synthesized and secreted by endothelial cells (8).ET-1 has also been shown to have potent hypertrophy-promoting effects in a variety of mammalian cells, including vascular smooth muscle cells, cardiomyocytes (13), and fibroblasts (25). Various models of cardiac hypertrophy have demonstrated increased ET expression and secretion in the heart (13). ET-1 has been shown to be a potent stimulus for the hypertrophy of neonatal rat ventricular myocytes (NRVM) in vitro (24). In addition, ET-1 increases cell contraction frequency (14) and protein synthesis and modulates stretch-induced ANP release (21,20) and gene expression (8,9,12,13,19). Skvorak et al...

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Evidence supporting a physiological role for proANP-(1–30) in the regulation of renal excretion

Cited by 29 publications

References 28 publications

Cardiac hormones for the treatment of cancer

Cardiac hormones for the treatment of cancer

Urodilatin: A better natriuretic peptide?

CytochromeP-450 metabolites in endothelin-stimulated cardiac hormone secretion

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