Atrial natriuretic factor: Structure and functional properties

Maack, Thomas; Camargo, M. J. F.; Kleinert, Hollis D.; Laragh, John H.; Atlas, Steven A.

doi:10.1038/ki.1985.54

Cited by 299 publications

(104 citation statements)

References 42 publications

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“…Twenty-five years later DeBold and colleagues discovered a potent and rapidly-acting natriuretic and vasorelaxing agent in extracts from rat heart atrium-the atrial natriuretic factor (ANF) [143]. In the kidney, ANF increases the glomerular filtration rate and decreases collecting duct sodium transport [144]. The glomerulus is a major target site for ANF.…”

Section: The Adaptive Role Of Prostaglandin Synthesismentioning

confidence: 99%

Cross‐talk between transmembrane signalling systems: a prerequisite for the delicate regulation of glomerular haemodynamics by mesangial cells

Pfeilschifter

1989

Eur J Clin Investigation

105

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Section: The Adaptive Role Of Prostaglandin Synthesismentioning

confidence: 99%

Cross‐talk between transmembrane signalling systems: a prerequisite for the delicate regulation of glomerular haemodynamics by mesangial cells

Pfeilschifter

1989

Eur J Clin Investigation

105

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“…Furthermore, it has become clear that ANP is closely connected to the renin-angiotensin-aldosterone system through various mechanisms including (1) inhibition of the release of renin (Kurtz et al, 1986), (2) opposition to the sodium retaining effect of angiotensin II (McMurray & Struthers, 1988), (3) blockade of the synthesis and release of aldosterone (Higuchi et al, 1986), (4) blockade of the sodium retaining effect of aldosterone (Mantero et al, 1987) and (5) opposition to the vasoconstrictor effect of angiotensin II (Maack et al, 1985). Despite this close relationship, few studies have been reported in the literature on the effects of blockade of the renin-angiotensin-aldosterone system by converting enzyme inhibitors on the pharmacological actions or plasma levels of ANP. It has been shown in Wistar rats that the natriuretic action of infusion of ANP is not influenced by pretreatment with captopril (Hirata et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

The effect of acute ACE inhibition on atrial natriuretic peptide.

Doorenbos

Brummelen

1989

Brit J Clinical Pharma

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1 The effect of acute angiotensin converting enzyme (ACE) inhibition on the plasma concentrations of atrial natriuretic peptide (ANP) was investigated in a single-blind placebo controlled crossover study in healthy volunteers. 2 Intravenous infusion of 2 mg cilazaprilat resulted in a significant and short lasting inhibition of ACE as evidenced by a decrease of plasma angiotensin II and an increase in plasma renin activity. 3 When compared with placebo cilazaprilat lowered diastolic pressure and increased heart rate significantly. 4 No effect of cilazaprilat was found on plasma ANP levels, suggesting that angiotensin II does not mediate ANP release.

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“…On the other hand, none of the main factors known to stimulate the renal PG biosynthesis (Levensson et al, 1982) seems to be clearly involved. An influence by angiotensin II appears unlikely since ANP administration would be expected to suppress rather to enhance renin release (Maack et al, 1985). Moreover, in our study, the subjects were salt-loaded and exhibited a low renin already to start with (Biollaz et al, 1987).…”

Section: Discussionmentioning

confidence: 83%

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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Atrial natriuretic factor: Structure and functional properties

Cited by 299 publications

References 42 publications

Cross‐talk between transmembrane signalling systems: a prerequisite for the delicate regulation of glomerular haemodynamics by mesangial cells

Cross‐talk between transmembrane signalling systems: a prerequisite for the delicate regulation of glomerular haemodynamics by mesangial cells

The effect of acute ACE inhibition on atrial natriuretic peptide.

Atrial natriuretic peptide and urinary prostaglandins in man.

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