Natriuretic Hormone: Current Status

Buckalew, Vardaman M.; Paschal-McCormick, Cheryl

doi:10.1159/000167989

Cited by 11 publications

(4 citation statements)

References 49 publications

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“…A corollary of this may be a physiological role for ANP in the acute regulation of plasma volume since, on release into circulation, it has been shown to possess diuretic and natriuretic properties in man (Solomon, Atherton, Bobinski et al 1988;McMurray, Seidelin & Struthers, 1989) and many animal models (Buckalew & Paschal-McCormick, 1989). In states of volume depletion, coincident with the stimulation of vasopressin secretion (Dunn, Brennen, Nelson & Robertson, 1973), ANP release appears to be inhib¬ ited (DeBold, 1979).…”

Section: Introductionmentioning

confidence: 99%

Plasma atrial natriuretic peptide in vasopressin deficiency the effects of acute water deprivation in rats

Burgess

Balment²

1992

Journal of Endocrinology

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Plasma concentrations of atrial natriuretic peptide (ANP) and other renally active hormones were measured in Long-Evans (LE) rats and vasopressin-deficient Brattleboro rats with diabetes insipidus (DI) in conditions of water repletion and deprivation, and in DI rats following chronic vasopressin replacement. In water-replete rats, vasopressin deficiency was associated with elevated circulating ANP and angiotensin II (AII) concentrations, while plasma adrenal steroid concentrations were depressed by comparison with LE rats. These differences were fully reversed after 7 days of vasopressin replacement in DI rats to restore normal water turnover. Water deprivation for 4 h had little effect on plasma tonicity or hormone profile in LE rats. In contrast, however, the unreplaced fluid loss during 4-h water deprivation in the DI rat was associated with a marked increase in plasma tonicity evident within 30 min. Plasma ANP concentrations fell substantially to levels below those in LE rats, coincident with a rise in adrenal steroid levels and independent of any clear change in AII. These changes in circulating ANP concentration were directly correlated with changes in plasma Na+ concentration, osmolality and tissue water content in the DI rats, underlining the importance of body fluid status in modulating the secretion of ANP. These data clearly show that plasma ANP concentration is increased in vasopressin deficiency, but emphasize the sensitivity of circulating hormone levels in vasopressin-deficient animals to acute changes in the state of hydration, underscoring the complex and labile interaction between body fluid and hormonal factors involved in the control of ANP secretion.

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Section: Introductionmentioning

confidence: 99%

Plasma atrial natriuretic peptide in vasopressin deficiency the effects of acute water deprivation in rats

Burgess

Balment²

1992

Journal of Endocrinology

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“…In fact, in a previous study of ours, a marked reduction of plasma natriuretic activity was found in cirrhotic patients before ascites was evident [3]. For the methodology applied in the above-mentioned experiment, it was probable that the na ture of the 'natriuretic substance' we isolated was com pletely different from ANP (molecular weight < 1,000 daltons) and quite near to other natriuretic factors known to have an hypertensive activity [40], Moreover, it could be theoretically possible that a re duced sensitivity of peripheral receptors to ANP might increase its plasma levels. This hypothesis seems to be sustained by a large number of observations [26,28,30] providing evidence for a reduced natriuretic response to ANP infusion.…”

Section: Discussionmentioning

confidence: 81%

“…This finding seems to be in contradiction not only with the underfilling hypothesis, but also with a hypotheti cal pathogenetic role of the natriuretic factor in sodium retention of cirrhosis. However, it is also known that plasma natriuretic activity is not only due to the ANP effect, but to many other substances, only in part chemically defined, than can modulate natriuretic activity by quite different mechanisms of action in different sets of physiological and pathological conditions [40], Therefore, a reduction in the plasma activity of some other natriuretic factor(s) could be in part counteracted by an increase of ANP levels. In fact, in a previous study of ours, a marked reduction of plasma natriuretic activity was found in cirrhotic patients before ascites was evident [3].…”

Section: Discussionmentioning

confidence: 99%

Atrial Natnuretic Peptide and Hemodynamic Changes after Concentrated Ascitic Fluid Reinfusion in Cirrhotic Patients

Cannella¹,

Mioni²,

Boscutti³

et al. 1993

Nephron

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In order to assess the role, if any, of atrial natriuretic peptide (ANP) and hemodynamic changes in diuretic response to concentrated ascitic fluid reinfusion (CAFR) in cirrhotic patients, we studied 10 patients with liver cirrhosis before and after aspiration, concentration and intravenous reinfusion of their ascitic fluid. Basal ANP levels were higher than in normal subjects, but not related to the degree of water and sodium excretion. CAFR induced a variable degree of ANP changes and diuretic response, and these two parameters were strictly correlated to each other. No major changes of cardiac output and systemic vascular resistances were observed after CAFR. In conclusion, the apparent resistance to ANP diuretic action observed in basal condition in cirrhotic patients seems to revert after expanding blood volume by CAFR.

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“…Since then, numerous in vivo and in vitro studies provided additional evidence to the existence of such "natriuretic hormones" (for reviews see Bricker et al 1975;de Wardener and Clarkson 1985;Buckalew and Paschal-McCormick 1989). Indeed, several studies reported the natriuretic activity of low-molecular-weight (<1000 Da) substances present in the plasma and urine of salt-and volume-loaded humans (Clarkson et al 1976;Epstein et al 1978) as well as in patients with chronic renal disease (Bourgoignie et al 1974;Bricker et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Renal effects of a novel endogenous natriuretic agent xanthurenic acid 8-o-β-d-glucoside in rats

et al. 2013

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Xanthurenic acid 8-o-β-d-glucoside is an endogenous derivative of tryptophan metabolism, isolated from urine of patients with chronic renal disease. This compound was suggested previously to act as a natriuretic hormone based on its ability to block short circuit currents in a frog skin assay and to induce a sustained natriuresis when injected into rats (C. D. Cain et al., Proc. Natl. Acad. Sci. USA 2007: 17873–17878). The present communication describes the effects of the compound on renal clearance and hemodynamic parameters in male Sprague–Dawley rats maintained on a normal salt (0.4–0.5%) diet. Intravenous administration of synthetic xanthurenic acid 8-o-β-d-glucoside in two consecutive incremental doses (6.3 and 31.5 nmol) resulted in a significant increase (P < 0.05), in urine flow (43.91 ± 6.31 μL/min vs. 10.54 ± 2.21 μL/min), absolute rate of sodium excretion (3.99 ± 0.95 μEq/min vs. 1.15 ± μEq/min), and percentage sodium excretion (1.63 ± 0.46% vs. 0.37 ± 0.12%, peak response vs. baseline, respectively). The natriuretic/diuretic effect was associated also with a significant increase in potassium excretion. These effects were not related to changes in renal hemodynamics or in arterial blood pressure. Pretreatment with the sodium channel blocker, amiloride, completely abolished the natriuretic and kaluretic actions of the compound. Administration of the xanthurenic acid derivative caused a dose-related increase in urinary nitrite/nitrate excretion. Moreover, under chronic nitric oxide blockade by l-NG-Nitro-Arginine-Methyl-Esther (l-NAME) sodium excretion was similar in rats treated or untreated with the compound. Our data demonstrate that xanthurenic acid 8-o-β-d-glucoside has significant diuretic/natriuretic and kaluretic properties. An intact amiloride-sensitive sodium channel is required for the renal effects of the compound. The data further suggest that the natriuretic effect is mediated in part by a nitric oxide-dependent mechanism.

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Natriuretic Hormone: Current Status

Cited by 11 publications

References 49 publications

Plasma atrial natriuretic peptide in vasopressin deficiency the effects of acute water deprivation in rats

Plasma atrial natriuretic peptide in vasopressin deficiency the effects of acute water deprivation in rats

Atrial Natnuretic Peptide and Hemodynamic Changes after Concentrated Ascitic Fluid Reinfusion in Cirrhotic Patients

Renal effects of a novel endogenous natriuretic agent xanthurenic acid 8-o-β-d-glucoside in rats

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