Optimization of atrial natriuretic factor radioimmunoassay

Sarda, Inder R.; Bold, M. L. de; Bold, Adolfo J. de

doi:10.1016/s0009-9120(89)80063-3

Cited by 69 publications

(30 citation statements)

References 11 publications

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“…Urinary cGMP concentrations were determined with a commercially available RIA kit (Dupont-NEN, Boston, MA). Plasma and cardiac tissue concentrations of immunoreactive (ir) ANF and BNP were determined by RIA using anti-rat ANF99-126 and anti-rat BNP64-95 serum, respectively, from Peninsula Laboratories, Inc. (Belmont, CA) (38). The antibodies used showed less than 0.01% crossreactivity between ANF and BNP.…”

Section: Assay Methodsmentioning

confidence: 99%

“…After plasma processing, the cartridges were washed with 20 ml of 0.1% trifluoroacetic acid (38), and then eluted with 3 ml of 60% acetonitrile in 0.1% trifluoroacetic acid. Tissue samples were homogenized in 10 vol of an extracting mixture consisting of 0.1 N HCl, 1.0 M acetic acid, and 1% NaCl, and centrifuged at 10,000 g for 30 min at 40C.…”

Section: Extraction Ofplasma and Tissue Samplesmentioning

confidence: 99%

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Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway.

Yokota

Bruneau²,

Bold³

et al. 1994

J. Clin. Invest.

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The mechanism underlying the mineralocorticoid escape phenomenon remains unknown. To assess the possible contribution of natriuretic peptides to mineralocorticoid escape, rats were injected with 5 mg deoxycorticosterone acetate for 3 d. Plasma atrial natriuretic factor (ANF) rose to twice basal levels and atrial ANF content decreased significantly by 24 h of treatment. This coincided with renal escape and with a significant increase in urinary cGMP excretion. Plasma ANF remained elevated and atrial ANF content continued to decline by 48 and 72 h while atrial ANF mRNA levels increased significantly only at 72 h. Plasma brain natriuretic peptide did not increase during escape although atrial brain natriuretic peptide mRNA levels increased significantly. Chronically administered HS-142-1 (HS), a specific antagonist of the guanylate cyclase-coupled natriuretic peptide receptors, significantly and dose-dependently impaired the escape phenomenon. The highest dose of HS completely suppressed the increase in urinary cGMP. Despite the continued suppression, partial escape was observed by the end of the observation period. HS alone influenced neither plasma nor tissue or urine parameters. These findings show that despite activation of atrial ANF, blockade of the guanylate cyclase-coupled natriuretic peptide receptors impairs the ability of the kidney to escape the Na+ retaining effect of excess mineralocorticoid in a dose-dependent fashion. Later-acting, unknown mechanisms eventually come into play to mediate the escape phenomenon through a guanylate cyclase-independent pathway. Therefore, ANF of cardiac origin appears to be a major factor initiating mineralocorticoid escape through a guanylate cyclase-dependent pathway. (J.

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Section: Assay Methodsmentioning

confidence: 99%

Section: Extraction Ofplasma and Tissue Samplesmentioning

confidence: 99%

Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway.

Yokota

Bruneau²,

Bold³

et al. 1994

J. Clin. Invest.

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“…Upon thawing, plasma samples were acidified by addition 100 l 1.0 N HCl/ml plasma and extracted with Sep-Pak C 18 cartridges (Millipore-Waters, Milford, MA). Radioimmunoassay was performed using the double antibody technique as previously described by Sarda et al (30).…”

Section: Plasma Samplesmentioning

confidence: 99%

“…ANF levels were determined in 100-l aliquot media samples using the double antibody RIA technique, as described by Sarda et al (30). Antisera against ANF 99 -126 (Peninsula Laboratories) were used.…”

Section: Anf Radioimmunoassaymentioning

confidence: 99%

Ras dexamethasone-induced protein 1 is a modulator of hormone secretion in the volume overloaded heart

McGrath

Ogawa

Bold

2012

American Journal of Physiology-Heart and Circulatory Physiology

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Because of the crucial role of the endocrine heart in maintaining homeostasis, considerable effort has been focused on the elucidation of the mechanistic underlying gene expression and secretion of the cardiac hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP). However, much remains to be determined regarding specific molecular events involved in cardiocyte secretory function. In this work, we identified genes involved in the transcriptional response of the endocrine heart to volume overload (VO) and signaling pathways involved in its regulation. To this end, the cardiac atrial and ventricular transcriptomes were analyzed in the heart of rats subjected to experimentally induced aorto-caval shunt VO. Pathway analysis revealed unique gene expression profiles in the VO atria for G-protein signaling, notably a significant downregulation of Ras dexamethasone-induced protein 1 (RASD1). In vitro, knockdown of RASD1 in the atrial-derived HL-1 cells, significantly increased ANF secretion. Concurrent knockdown of RASD1 and its effectors Gαo1 or Gβ1γ2 abrogated the endocrine response, demonstrating a previously unknown negative modulator role for RASD1. RASD1 thus emerges as a tonic inhibitor of ANF secretion and illustrates for the first time the concept of inhibitory protein regulators of ANF release. The novel molecular function identified herein for RASD1 is of considerable importance given its therapeutic implications for cardiovascular disease.

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“…Standard competitive RIA was performed to quantify ANF according to a previously published protocol (43).…”

Section: Animalsmentioning

confidence: 99%

Phospholipase C signaling tonically represses basal atrial natriuretic factor secretion from the atria of the heart

Chang

McGrath

Bold

2013

American Journal of Physiology-Heart and Circulatory Physiology

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The cardiac hormone atrial natriuretic factor (ANF or ANP) plays significant, well-established roles in a large number of physiological and pathophysiological processes, including water and electrolyte balance, blood pressure regulation, and cardiovascular growth. Understanding the regulation of its production and secretion by atrial cardiomyocytes is incomplete. We have previously established a significant role of Gi/o protein signaling in modulating ANF secretion as promoted by stretch of the atrial myocardium. In the present study, we investigated the role of Gq protein signaling and its relationship to Gi/o protein signaling using pharmacological manipulation of proximal effectors of Gαq in an ex vivo model of spontaneously beating rat atria. Phospholipase C (PLC) and protein kinase C (PKC) inhibitors dramatically increased basal secretion of ANF. Furthermore, although atrial wall stretch is a potent stimulus for secretion, stretch unexpectedly reduced ANF secretion to basal levels under PLC and PKC inhibitory conditions. Inhibition of the inositol triphosphate receptor did not appear to affect basal secretion but dose-dependently blocked stretch-secretion coupling. The results obtained demonstrate that the PLC and PKC signaling cascades play important albeit unexpected roles in the regulation of basal and stimulated ANF secretion and suggest interplay between the Gq and Gi/o protein signaling pathways.

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Optimization of atrial natriuretic factor radioimmunoassay

Cited by 69 publications

References 11 publications

Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway.

Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway.

Ras dexamethasone-induced protein 1 is a modulator of hormone secretion in the volume overloaded heart

Phospholipase C signaling tonically represses basal atrial natriuretic factor secretion from the atria of the heart

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