Atrial natriuretic peptide, right atrial pressure, and sodium excretion rate in the rat

Fried, T. A.; Ayon, M. A.; McDonald, George G.; Lau, Alisa; Inagami, Tadashi; Stein, Janice Gross

doi:10.1152/ajprenal.1987.253.5.f969

Cited by 16 publications

(6 citation statements)

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“…Normal rabbit serum, which had no effect on circulating ANP concentrations, produced no such changes in renal function. These results, which are similar to those shown for mammals (Hirth et al 1986, Fried et al 1987), convincingly demonstrate a regulatory role for endogenous ANP in the renal response to volume expansion in birds and hence in the mainte¬ nance of salt and fluid balance of this animal group.…”

Section: Anti-anp and Renal Excretionsupporting

confidence: 86%

Role of endogenous atrial natriuretic peptide in volume expansion diuresis and natriuresis of the Pekin duck

Gray

1994

Journal of Endocrinology

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Polyclonal antibodies raised in a rabbit against avian atrial natriuretic peptide (ANP) were shown to reduce circulating endogenous ANP levels in Pekin ducks by more than 90%, and were subsequently used to investigate the role of this peptide in volume expansion diuresis and natriuresis. Conscious birds, undergoing a steady-state diuresis and natriuresis maintained by an i.v. infusion of hypotonic saline at a rate of 0.7 ml/min, responded to ANP antiserum (anti-ANP) with an immediate 30% reduction in urine flow rate and sodium excretion which lasted for about 30 min. Plasma arginine vasotocin levels were not changed by anti-ANP whereas circulating angiotensin II concentrations increased immediately following the administration of anti-ANP. Serum from non-immunized normal rabbits produced no changes in the renal and plasma parameters monitored. The results show that the high circulating levels of endogenous ANP associated with volume expansion promote renal salt and fluid excretion and thus have a major physiological role in avian volume homeostasis.

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Section: Anti-anp and Renal Excretionsupporting

confidence: 86%

Role of endogenous atrial natriuretic peptide in volume expansion diuresis and natriuresis of the Pekin duck

Gray

1994

Journal of Endocrinology

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“…ANF antibodies were shown to blunt the natriuresis of large acute blood volume expan sion in anesthetized rats [10], These results have been confirmed by Sakata et al [92] in rats made autoimmune to ANF, and by Fried et al [103] in rats given exogenous anti-ANF antibodies. Sakata et al [92] showed, however, that autoimmune rats increased UNaV in the expected fashion when studied in the conscious state.…”

Section: Evidence From Studies Designed To Block the Release Or Effecmentioning

confidence: 61%

Natriuretic Hormone: Current Status

Buckalew¹,

Paschal-McCormick²

1989

Am J Nephrol

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“…Only urodilatin paralleled the natriuresis induced by balloon dilatation, whereas CDD/ANP-99-126 showed no positive correlation. However, although contradictory results exist that attribute an important role to CDD/ANP-99-126 during dietary sodium load [24] and increasing volume load [ 18], a number of investigators suggest that urodilatin, not CDD/ANP-99-126, is responsible for the altered renal sodium excretion. Therefore, urodilatin may be more important than CDD/ANP-99-126 in POD.…”

Section: Is Urodilatin Involved In Postobstruetive Diuresis?mentioning

confidence: 99%

The renal paracrine peptide system ? possible urologic implications of urodilatin

et al. 1996

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Cardiodilatin/atrial natriuretic peptide (CDD/ ANP) is a hormone system of great clinical importance. The prohormone CDD/ANP-1-126 is a peptide synthesized in the heart and cleaved during exocytosis into the circulating form CDD/ANP-99-126. Urodilatin (CDD/ ANP-95-126) is a homologue natriuretic peptide that differs from CDD/ANP-99-126 by four amino acids. Whereas CDD/ANP-99-126 circulates in blood plasma and is not excreted into the urine, urodilatin is detected only in urine. Urodilatin exerts its renal effects in a paracrine fashion. After its secretion from cells in the distal tubule, it interacts with luminally located receptors in the collecting duct, resulting in increased diuresis and natriuresis. Results suggest that urodilatin plays an important role in the physiologic regulation of fluid-balance and sodium homeostasis. Pharmacology studies reveal significant differences when urodilatin and CDD/ANP-99-126 are given intravenously, showing that stronger diuresis and natriuresis are induced by urodilatin as compared with those induced by CDD/ANP-99-126. Clinical studies indicate the prophylactic and therapeutic effect of urodilatin in patients suffering from acute renal failure following heart and liver transplantation. A significant reduction in requirements for hemodialysis/hemofiltration can be achieved using urodilatin. Postobstructive diuresis and natriuresis is probably due to a defective urinary concentrating mechanism and is usually resistant to treatment with antidiuretic hormone. The distal tubule and collecting duct have often been considered to be the site of altered sodium and water excretion following relief of obstruction. Since circulating CDD/ANP-99-126 levels are markedly elevated during obstruction and decrease upon relief of the obstruction, natriuretic peptides may play an important role in this clinical feature. On the basis of recent findings attributing an important role in sodium homeostasis to urodilatin in contrast to CDD/ANP-99-126, future studies have to clarify whether urodilatin, not CDD/ANP-99-126, might be responsible for the altered renal sodium excretion observed in postobstructive diuresis. In the past decade a considerable amount of research has led to the identification and characterization of hormones of the natriuretic peptide family [13]. These peptides are involved in the regulation of salt and water homeostasis. The prototype of the natriuretic hormones is cardiodilatin/atrial natriuretic peptide (CDD/ANP), or A-type natriuretic peptide. CDD/ANP is primarily produced in the heart [6]. It is synthesized as a precursor molecule, CDD/ ANP-1-126, in specific granules in atrial myoendocrine cells [15]. The prohormone, upon appropriate stimuli for release, is cleaved into the C-terminus CDD/ANP-99-126 and excreted into the circulation via exocytosis [16]. Further members of the natriuretic peptide family are brain natriuretic peptide (BNP, or B-type natriuretic peptide) [45] and C-type natriuretic peptide (CNP) [46]. All the members of this family share many common feat...

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Atrial natriuretic peptide, right atrial pressure, and sodium excretion rate in the rat

Cited by 16 publications

References 0 publications

Role of endogenous atrial natriuretic peptide in volume expansion diuresis and natriuresis of the Pekin duck

Role of endogenous atrial natriuretic peptide in volume expansion diuresis and natriuresis of the Pekin duck

Natriuretic Hormone: Current Status

The renal paracrine peptide system ? possible urologic implications of urodilatin

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