Atrial natriuretic peptide: what is the excitement all about?

Anderson, J. V.; Bloom, Stephen R.

doi:10.1677/joe.0.1100007

Cited by 57 publications

(26 citation statements)

References 71 publications

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“…Abbreviations used in this paper: ANF, atrial natriuretic factor; APIII, atriopeptin III (Ser5-Tyr2g); hANF, human ANF (Ser1-Tyr28); 1251, iodotyrosyl28; rAIB13 , rat aminoisobutyric acid; rANF, rat ANF (Ser1-Tyr28). (1)(2)(3)(4). After secretion, ANF binds to cell-surface receptors to elicit these physiological responses.…”

Section: Introductionmentioning

confidence: 99%

Clearance and early hydrolysis of atrial natriuretic factor in vivo. Structural analysis of cleavage sites and design of an analogue that inhibits hormone cleavage.

Condra¹,

Leidy²,

Bunting³

et al. 1988

J. Clin. Invest.

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This study examines the clearance and early hydrolysis of atrial natriuretic factor (ANF) in vivo. Radiolabeled ANF was cleared from the circulation of the rat with biphasic kinetics; the majority (90%) of ANF cleared with a tl/2 of 15 s, the remaining peptide was cleared with a t1/2 of 5 min. Microsequence analysis of ANF peptides recovered from the circulation of rats revealed five major degradation products of the intact hormone. The first cleavage occurred between amino acids 12 and 13 of the hormone and would inactivate ANF. Over time, additional fragments of the hormone were generated, including fragments of 6, 7, 21, and 24 amino acids in length.Whole body radioautography of rats injected with I123II-ANF revealed the kidney as a predominant organ involved in clearance of ANF. Subsequent amino acid sequence analyses of radiolabeled ANF exposed to the kidney in vivo indicated that this organ generated four of the five major hydrolysis products observed in circulation, namely, the 6, 7, 16, and 21 amino acid fragments of the hormone. In an attempt to stabilize ANF in vivo, a synthetic analogue of the hormone was prepared that contained the amino acid analogue, aminoisobutyric acid, substituted at position 13. This analogue completely abolished the in vivo cleavage of ANF at this site. These studies demonstrate the usefulness of a protein chemistry approach in characterizing hormone metabolism in vivo and designing analogues with enhanced in vivo stability to cleavage.

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Section: Introductionmentioning

confidence: 99%

Clearance and early hydrolysis of atrial natriuretic factor in vivo. Structural analysis of cleavage sites and design of an analogue that inhibits hormone cleavage.

Condra¹,

Leidy²,

Bunting³

et al. 1988

J. Clin. Invest.

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“…In these patients, the elevation of ANF is reflective of ductal flow. (Pediatr Res 27:137-139, 1990) Abbreviations release of renin, aldosterone, and vasopressin (4,5). In neonates with RDS (6) plasma concentration of ANF is increased compared to normal newborns.…”

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confidence: 99%

Correlation of Patent Ductus Arteriosus Shunting with Plasma Atrial Natriuretic Factor Concentration in Preterm Infants with Respiratory Distress Syndrome

et al. 1990

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ABSTRACT. The concentration of plasma atrial natriuretic factor (ANF) and the mechanism for its secretion were investigated in 17 preterm infants with respiratory distress. Their mean gestational age was 29 wk and wt 1250 g. The infants were followed during the first week of life by sequential Doppler ultrasound studies. Ductal openness versus closure and amount of ductal flow were correlated with plasma ANF concentrations. In a subset of 10 infants, sequential Doppler color flow mapping was used to quantify the ductal flow. During the first 72 h, plasma ANF was high, 361 pg/mL; it decreased to 96 pg/mL by the end of the 1st wk. (4, 5). In neonates with RDS (6) plasma concentration of ANF is increased compared to normal newborns. In these patients the peak plasma ANF concentration coincides with the diuretic phase found between 18 to 43 h of age (7).To clarify the association of ANF secretion and hemodynamic changes in preterm infants with RDS, we determined the Qp/Qs ratio and ductal closure by CFM with a method we developed previously (8). The focus of this study was the effect of ductal flow on plasma ANF concentration in preterm infants with RDS. MATERIALS AND METHODSSeventeen preterm infants (26-33 wk gestation) with birth wt of 0.66 to 1.95 kg (mean 1.25 kg) developed clinical signs and radiographic features consistent with RDS. Nine infants were delivered by caesarean section, and Apgar scores ranged from 3 to 8 at 1 min (mean 6) and from 6 to 9 at 5 min (mean 8). In 15 infants, analysis of amniotic fluid obtained within 24 h before birth revealed lecithin/sphingomyelin ratios less than 2.0 with absence of phosphatidylglycerol, and in two remaining infants tracheal aspirates obtained at birth contained no phosphatidylglycerol. These findings and the clinical course were consistent with severe RDS. This was further substantiated by calculating the arteriolar/alveolar oxygen tension ratio (9) at 6 h of age (0.17 5 0.08: mean + SD), which confirmed the disturbance in gas ANF, atrial natriuretic factor exchange and the requirement for supplemental oxygen and CFM, color flow mapping mechanical ventilation. Infants included in this study had no LA/Ao ratio, left atrial to aortic root diameter evidence of chorioamnionitis, congenital infection, or major PDA, patent ductus arteriosus malformations.Qp/Qs, pulmonic to systemic blood flow ratio Blood samples of 0.5 mL were drawn through umbilical artery catheters into ice-cold EDTA-containing tubes that were rapidly RDS, respiratory distress syndrome centrifuged at 300 x n. Plasma was sevarated for immediate freezingand stored at -3 0 "~ for up to 3 mo before ANF analysis. From each patient during the 1st wk of life, one to four samples were taken within 3 h of a CFM study. RIA was camed out as ANF is a secreted from the atria of the heart (1). In term previously described (10). Sensitivity of the method is 5 pg/mL. newborns plasma concentration of ANF is increased during the The intra-and interassay coefficients of variation are 10.6 and first 2 to 4 d of life (2,...

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“…20 Conceivably, in some circumstances ANF could cause reciprocal changes in cardiac output and total peripheral resistance, while arterial blood pressure changes very little. Indeed, when ANF was administered as a 125-ng/kg bolus followed by 25 ng • min" 1 • kg" 1 , stroke volume was significantly decreased 30 minutes after the start of infusion, but arterial blood pressure was not different from control level. 22 Plasma ANF concentration increased from 54 to 457 pg/ml and was stated to be within the physiological range, although data in that regard were not reported.…”

Section: Humansmentioning

confidence: 94%

“…Using plasma extract, a majority of studies show mean values for basal plasma ANF of healthy volunteers in the range of 10 to 60 pg/ml. 1 However, much variation still exists among laboratories, with individual values ranging as low as 2 to 12 pg/ml 3 or as high as 27 to 152 pg/ml 6 for basal levels of plasma ANF in healthy subjects. Differences in procedures for collecting and storing samples, extraction recoveries, specificities of antibodies, and purities of standards probably account for these disparities.…”

Section: Physiological Effects Of Anfmentioning

confidence: 99%

“…Rat ANF (101-126) was infused by osmotic pumps into rats with various forms of hypertension at approximately 5 ng • min" 1 • kg" 1 . Systolic blood pressure, measured indirectly, decreased gradually over 7 days in spontaneously hypertensive rats (SHR) 25 and in rats with one-kidney, one clip 26 or two-kidney, one clip 27 renal hypertension.…”

Section: Prolonged Infusionmentioning

confidence: 99%

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An update on the physiology of atrial natriuretic factor.

Trippodo

1987

Hypertension

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SUMMARY The atrial natriuretic factor (ANF) has pharmacological actions resulting in lower atrial and arterial pressures. Atrial distention stimulates ANF release, suggesting that ANF is an effector limb of a feedback loop for controlling cardiac filling pressure. To test this hypothesis it will be necessary to determine whether physiological atrial distention releases ANF in sufficient amounts to exert biological actions. Immunoblockade of endogenous ANF and attenuation of ANF release by atrial ablation inhibited volume-induced natriuresis in rats. Infusion of ANF in rats at doses mimicking those observed during experimental volume expansion produced a natriuresis sufficient to partly account for the volume-induced response. Infusion of ANF at doses expected to change plasma ANF levels minimally decreased arterial pressure in hypertensive rats over 7 days. In dogs, some studies suggest that increased plasma ANF levels following experimental changes in atrial pressure were not sufficient to exert acute cardiovascular or renal actions, whereas others support such a notion and indicate that ANF inhibited barostimulated renal renin release. This last action could alter arterial pressure in the long term by allowing sodium equilibrium at lower renal arterial pressure. Infusion of ANF in humans that produced plasma levels in the upper physiological range caused increased sodium excretion and decreased plasma renin activity. Although data are exiguous, justifying neither acceptance nor rejection of the hypothesis that ANF functions physiologically to regulate body fluid volume and arterial pressure, the current evidence slightly favors acceptance. T HIS discussion reviews recent data relating to the possible physiological relevance of the atrial natriuretic factor (ANF) as a regulator of urinary sodium excretion and arterial blood pressure.

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Atrial natriuretic peptide: what is the excitement all about?

Cited by 57 publications

References 71 publications

Clearance and early hydrolysis of atrial natriuretic factor in vivo. Structural analysis of cleavage sites and design of an analogue that inhibits hormone cleavage.

Clearance and early hydrolysis of atrial natriuretic factor in vivo. Structural analysis of cleavage sites and design of an analogue that inhibits hormone cleavage.

Correlation of Patent Ductus Arteriosus Shunting with Plasma Atrial Natriuretic Factor Concentration in Preterm Infants with Respiratory Distress Syndrome

An update on the physiology of atrial natriuretic factor.

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