Renal and systemic effects of synthetic atrial natriuretic factor

Seymour, A A; Blaine, Edward H.; Mazack, E K; Smith, Shaler G.; Stabilito, Inez I.; Haley, Anne B.; Napier, Mary E.; Whinnery, M. A.; Nutt, Ruth F.

doi:10.1016/0024-3205(85)90283-8

Cited by 125 publications

(34 citation statements)

References 15 publications

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“…In addition, urinary cGMP responses were measured since earlier studies have indicated that cGMP mediates most, if not all, of the depressor and renal responses to ANF. 26 This conclusion is supported by evidence that biologically active ANFs stimulated cGMP levels in a variety of isolated vascular preparations, including cultured aortic endothelial cells, 35 and humans. 37 -38 In anesthetized dogs, 35 urinary cGMP excretion surpassed the filtered load of the cyclic nucleotide during intrarenal infusions of ANF-(101-126), and arterial cGMP load exceeded renal venous efflux, suggesting that urinary cGMP was derived from both renal and nonrenal sources.…”

Section: Discussionmentioning

confidence: 91%

“…26 This conclusion is supported by evidence that biologically active ANFs stimulated cGMP levels in a variety of isolated vascular preparations, including cultured aortic endothelial cells, 35 and humans. 37 -38 In anesthetized dogs, 35 urinary cGMP excretion surpassed the filtered load of the cyclic nucleotide during intrarenal infusions of ANF-(101-126), and arterial cGMP load exceeded renal venous efflux, suggesting that urinary cGMP was derived from both renal and nonrenal sources. Because other workers 26 have found that the time course of urinary cGMP excretion coincided more closely with the biological responses to ANF than did plasma cGMP levels, the rate of urinary cGMP excretion was believed to most accurately reflect ANF activity in vivo.…”

Section: Discussionmentioning

confidence: 91%

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Potentiation of renal effects of atrial natriuretic factor-(99-126) by SQ 29,072.

Seymour¹,

Fennell²,

Swerdel³

1989

Hypertension

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Depressor and renal activities of atrial natriuretic factor-(99-126) were determined in conscious, unrestrained spontaneously hypertensive rats treated with a neutral endopeptidase inhibitor, SQ 29,amino]heptanoic acid). SQ 29,072 (100 /tmol/kg i.v.) prolonged the transient depressor effects of the peptide for as long as 2 hours. During the first hour after 3, 10, and 30 nmol/kg atrial natriuretic factor, urinary excretion of cyclic 3'5' guanosine monophosphate was significantly increased by 9.2±3.4, 13.0±2.2, and 12.7±4.2 nmol/kg/hr, respectively, in vehicle-treated rats and by 26.9±7.9, 52.1±11.1, and 46.4±12.2 nmol/kg/hr, respectively, in rats given 100 /tmol/kg SQ 29,072. During the first hour after 3 and 10 nmol/kg atrial natriuretic factor-(99-126), the sodium loss was 161±56 and 139±42 /teq/kg/hr in vehicle-treated rats and was significantly greater (694±316 and l,038±135 /teq/kg/hr) in rats given 100 /tmol/kg SQ 29,072. After administration of 3, 10, and 30 /tmol/kg SQ 29,072, the area over the curves of the depressor responses to 3 nmol/kg of the peptide increased from 297±70 to 306±108, 440±143, and 669±186 mm Hgmin, respectively, while the concurrent natriuretic responses rose from 161±56 to 250±88,332±142, 464±164, and 694±316 /teq/kg/hr. In summary, the neutral endopeptidase inhibitor SQ 29,072 increased the magnitudes and especially the durations of the depressor, natriuretic, and cyclic guanosine monophosphate responses to exogenous atria] natriuretic factor-(99-126) in conscious spontaneously hypertensive rats, presumably by inhibition of degradation of atrial natriuretic factor in vivo. In conclusion, neutral endopeptidase inhibition offers an important new technique for enhancement and prolongation of the biological lifetime of atrial natriuretic factor. (Hypertension 1989;14:87-97)

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 91%

Potentiation of renal effects of atrial natriuretic factor-(99-126) by SQ 29,072.

Seymour¹,

Fennell²,

Swerdel³

1989

Hypertension

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“…No effect of ANF on CAMP level was observed in single nephron segments and glomeruli [21], or in arterial plasma following infusion of ANF into canine renal artery [22] or in isolated rabbit aortic segments [8]. On the other hand, in murine tumour Leydig cells [16] and in the rat pituitary [23], a marked inhibitory effect of ANF on CAMP formation has been reported.…”

Section: Discussionmentioning

confidence: 99%

Testosterone production by mouse Leydig cells is stimulated in vitro by atrial natriuretic factor

Mukhopadhyay¹,

Bohnet²,

Leidenberger³

1986

FEBS Letters

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The synthetic atria1 peptides, rat atria1 natriuretic peptide, atriopeptin I and atriopeptin II, stimulated testosterone production by mouse Leydig cells in a time-and concentration-dependent manner. The maximum stimulation of the steroidogenesis in response to the peptides was 6lo-fold over the basal level, as compared with 20-24-fold stimulation obtained with saturating concentrations of hCG. The stimulation of steroidogenesis by the most potent peptide, atriopeptin II, was markedly enhanced in the presence of the phosphodiesterase inhibitor, 3-isobutyl-I-methylxanthine, suggesting an involvement of cyclic nucleotides. However, neither basal nor hCG-stimulated levels of CAMP were altered by the peptide, though testosterone production in response to submaximal concentrations of hCG was increased in the presence of atriopeptin II. The nature of the second messenger involved and the mechanism of action of the atria1 peptides may by elucidated by further research in progress. (Mouse Leydig cell) Atria1 natriuretic factorTestosterone production cyclic AMP

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“…The mode of action of ANF on kidney function is still debated [7]. The hormone appears to enhance directly the glomerular filtration rate and both sodium and water filtration fractions [ 15,161. An inhibitory effect on tubular reabsorption has also been proposed [ 16,171. Specific high-affinity receptor sites have been documented in aorta [18], adrenal cortex [19], posterior lobe of the pituitary gland [14] and in kidney cortex [ 181.…”

Section: Introductionmentioning

confidence: 99%

Distribution of atrial natriuretic factor receptors in dog kidney fractions

1985

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Specific receptors for atria1 natriuretic factor were studied in purified glomeruli, proximal tubules, thick ascending limbs of Henle's loops and collecting ducts from dog kidney. Glomeruli contain the highest concentration of receptor sites (pK = 9.9, B,,,, = 200 fmol/mg protein), followed by collecting ducts (pK = 9.4, B mai = 150 fmol/mg). Low levels of receptor sites were also detectable in thick ascending limbs of Henle's loops (pK = 9.4, B,,, = 36 fmol/mg) while proximal tubules were completely devoid of specific binding sites. These results indicate that the glomeruli appear to be the primary site of interaction of artrial natriuretic factor in kidney cortex but that it might also act in the medulla on lower nephron tubular function. Atria1 natriuretic factor Vasoactive peptide Peptide receptor Glomerular function Tubular function (Dog kidney)

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Renal and systemic effects of synthetic atrial natriuretic factor

Cited by 125 publications

References 15 publications

Potentiation of renal effects of atrial natriuretic factor-(99-126) by SQ 29,072.

Potentiation of renal effects of atrial natriuretic factor-(99-126) by SQ 29,072.

Testosterone production by mouse Leydig cells is stimulated in vitro by atrial natriuretic factor

Distribution of atrial natriuretic factor receptors in dog kidney fractions

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