Atrial natriuretic factor has a direct, prostaglandin-independent action on kidneys

Keeler, R.

doi:10.1139/y82-155

Cited by 101 publications

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“…Since no correlations could be found between the urinary excretion of any PG and the natriuresis, it appears unlikely that renal PGs are involved in the natriuretic effect of ANP. This finding confirms the results obtained in humans (Miyamori et al, 1987) and animals (Keeler, 1982;Salazar et al, 1988) demonstrating that pharmacological blockade of PG biosynthesis by cyclo-oxygenase inhibition fails to attenuate the natriuresis elicited by ANP infusion. In contrast to natriuresis, the ANP-induced diuresis might rely partly upon the stimulation of renal PG biosynthesis.…”

Section: Discussionsupporting

confidence: 91%

“…Indeed, among the four PGs studied, only the two most effective upon the water excretion were found closely related to the UFR. Although the mechanism underlying their possible contribution remains unclear, this would confirm findings by Keeler (1982) who reported that inhibition of the PG biosynthesis attenuated the ANP induced diuresis.…”

Section: Discussionsupporting

confidence: 87%

“…Since infusion of PGE2 (Tannenbaum et al, 1975) and PGI2 (Gullner et al, 1980), results in an increased sodium and water excretion, it was suggested that PGs could be involved in the renal effects of ANP. However, the failure of cyclo-oxygenase inhibitors to decrease the ANP-induced natriuresis (Keeler, 1982;Salazar et al, 1988) argues against such a mechanism and strongly suggests that, in animals, renal PGs are presumably not involved in the effects of ANP. In man, such a conclusion needs to be confirmed since the evolution of renal PGs following ANP administration has not been yet described in healthy subjects and moreover the reported results differ from those obtained in animals.…”

Section: Introductionmentioning

confidence: 99%

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Atrial natriuretic peptide and urinary prostaglandins in man.

Benzoni¹,

Geoffroy²,

Waeber³

et al. 1989

Brit J Clinical Pharma

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1 In order to assess the effects of atrial natriuretic factor on the renal biosynthesis of prostaglandins (PG), the urinary excretion of PGE2, PGF20,, 6-keto-PGF10, and thromboxane (Tx)B2 were followed in eight salt-loaded healthy volunteers infused for 2 h with a non hypotensive dose of human atrial natriuretic peptide (hANP, 0.7 nmol min-1).2 Within 1 h, hANP, infusion produced a marked increase in the urinary PG output, especially of PGE2 and 6-keto-PGF10, (188 ± 21% and 202 ± 24% of the pre-infusion values respectively), followed by a significant decrease during the recovery period. 3 No correlations could be uncovered between the urinary excretion of sodium and that of any of the PGs. In contrast, during the infusion of hANP, the urinary output of PGE2 and of 6-keto-PGF10, was found positively related to the urinary flow rate (r = 0.42; P < 0.05; n = 32 and r = 0.43; P < 0.05; n = 32 respectively) as well as during the recovery period (r = 0.66, P < 0.001; n = 32 and r 0.55; P < 0.01; n = 32 respectively). 4 It was concluded that, in man, infusion of a non hypotensive dose of hANP is followed by a rise in urinary PG excretion presumably reflecting enhanced renal PG biosynthesis. This increased urinary PG excretion does not seem to be involved in the natriuretic action of hANP but might participate to its diuretic effect.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Atrial natriuretic peptide and urinary prostaglandins in man.

Benzoni¹,

Geoffroy²,

Waeber³

et al. 1989

Brit J Clinical Pharma

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“…This finding suggests that the increase in prostaglandin excretion seen with the infusion of ANF under control conditions is not mediating the natriuresis. Keeler 17 also has shown that the natriuretic effect of ANF is not prostaglandin-mediated.…”

Section: Discussionmentioning

confidence: 99%

Role of prostaglandins in mediating the renal effects of atrial natriuretic factor.

et al. 1988

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SUMMARY Tbe natriuretk response to the intrarenal administration of atrial natriuretic factor (ANF)is accompanied by an increase in tbe synthesis of prostaglandins and by a redistribution of renal blood flow from the superficial to the deep cortex. This study was undertaken to define whether prostaglandins mediate the ANF-induced redistribution of renal blood flow and if prostaglandins and renal blood flow redistribution contribute to the natriuretic actions of ANF. In anesthetized dogs, the Intrarenal administration of indomethadn (10 jtg/kg/min) or the intravenous administration of meclofenamate (5 mg/kg) completely prevented the sixfold and twofold increments in urinary prostaglandin E 2 and 6-keto-prostaglandin F l a excretion, respectively; it also abolished the redistribution of renal blood flow to the deep cortex. However, ANF induced a similar natriuresis before (from 53 ± 17 to 281 ± 48 /tEq/min) and after (from 45 ± 13 to 273 ± 60 /iEq/min) the administration of prostaglandin synthesis inhibitors. It is concluded that the ANF-induced redistribution of renal blood flow to the deep cortex is prostaglandinmediated but that neither redistribution nor increased prostaglandin synthesis Is an important mediator of ANF's natriuretic action. (Hypertension 12: 274-278, 1988) KEY WORDS • atrial natriuretic factor • intrarenal blood flow distribution • prostaglandin synthesis inhibitors • sodium excretionW E have recently found that the natriuretic response to the intrarenal infusion of atrial natriuretic factor (ANF) at doses that do not alter mean arterial pressure (MAP), renal blood flow (RBF), or glomerular filtration rate (GFR) is accompanied by a significant increase in urinary excretion of prostaglandins and by a redistribution of RBF from the superficial to the juxtamedullary cortex.1 Previous studies have shown that enhanced prostaglandin synthesis or selective prostaglandin infusion increases juxtamedullary cortical flow.2 -5 Others have shown that blockade of prostaglandin synthesis decreases juxtamedullary cortical flow more than superficial cortical flow. 5 -7 Increases in medullary flow have been shown to produce natriuresis, 8 -9 as has increased prostaglan-

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“…The natriuretic effect of atrial extracts is now well documented (DeBold et al, 1981;Keeler, 1982;Trippodo et al, 1983). Furthermore, the factor producing the natriuretic effect ('atrial natriuretic factor' (ANF), a peptide containing an active portion of about 26 amino acid groups) has now been synthesized Thibault et al, 1984;Kangawa & Matsuo, 1984;Seidman et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

Atrial natriuretic factor causes specific relaxation of rat renal arcuate arteries

Aalkjær

Mulvany²,

Nyborg

1985

British J Pharmacology

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1 We have investigated the effect of a synthetic 'atrial natriuretic factor' (ANF) on induced tone in rat isolated renal arcuate arteries (lumen diameter ca. 250 Im), and compared this with the effects of synthetic ANF on resistance vessels of similar size taken from the mesenteric, femoral, cerebral and coronary vasculature. 2 Synthetic ANF was found to cause relaxation of the renal vessels when these were sub-maximally activated with K+, noradrenaline or 5-hydroxytryptamine, but had no effect on the responses of the other vessels to these agonists. Synthetic ANF had a near maximal effect (65% relaxation) at 100 nM, with an IC50 of 7.9 nm. The relaxant effect of synthetic ANF on the renal vessels was fully maintained for at least 15 min.3 Hydrallazine (100 gM) caused relaxation of renal vessels (47%) and coronary vessels (42%), but had no effect on the other vessel types. By contrast, sodium nitroprusside (1 gM) relaxed all vessel types.4 The relaxant action of synthetic ANF on the renal vessels was seen in the presence of ouabain (1 mM), propranolol (1 JM), phentolamine (1 LM), atropine (1 JM) and felodipine (1 nM). 5 In the renal vessels, synthetic ANF had no effect on membrane potential, measured with intracellular electrodes, despite the simultaneously measured relaxation.6 Synthetic ANF had no effect on the efflux of 22Na' in either renal or mesenteric vessels.7 The results demonstrate that synthetic ANF has a specific and prolonged relaxant effect on renal small arteries, and are consistent with this effect being mediated through specific receptors.

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Atrial natriuretic factor has a direct, prostaglandin-independent action on kidneys

Cited by 101 publications

References 0 publications

Atrial natriuretic peptide and urinary prostaglandins in man.

Atrial natriuretic peptide and urinary prostaglandins in man.

Role of prostaglandins in mediating the renal effects of atrial natriuretic factor.

Atrial natriuretic factor causes specific relaxation of rat renal arcuate arteries

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