Effect of atrial natriuretic peptide and on atriopeptins on the human isolated bronchus. Comparison with the reactivity of the guinea-pig isolated trachea

Candenas, Luz; Naline, Emmanuel; Puybasset, Louis; Devillier, Philippe; Advenier, C.

doi:10.1016/0952-0600(91)90062-8

Cited by 16 publications

(11 citation statements)

References 23 publications

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“…We completely agree with Candenas et al [30] and Labat et al [31], who suggested that there are no receptors for BNP on human airway smooth muscle and, consequently the We must highlight that we have used isolated bronchi from non atopic patients undergoing surgery because of lung cancer, whereas human recombinant BNP (nesiritide) is a potent bronchodilator in asthmatic patients [29]. These findings fit with the observation of Ohbayashi et al [20], who reported that ANP and BNP failed to relax guinea pig airways but both peptides inhibited antigen-induced bronchoconstriction in sensitized animals, suggesting that natriuretic peptide receptors might be expressed on airway smooth muscle during an inflammatory process.…”

Section: Article In Presssupporting

confidence: 93%

Relaxant effect of brain natriuretic peptide in nonsensitized and passively sensitized isolated human bronchi

Matera

Calzetta

Parascandolo

et al. 2009

Pulmonary Pharmacology & Therapeutics

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Section: Article In Presssupporting

confidence: 93%

Relaxant effect of brain natriuretic peptide in nonsensitized and passively sensitized isolated human bronchi

Matera

Calzetta

Parascandolo

et al. 2009

Pulmonary Pharmacology & Therapeutics

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“…It should be noted from these data, however, that lung parenchyma was very much less responsive than trachea [7], and that the response to ANP showed a degree of species dependence [7,19]. Earlier studies using atriopeptins failed to show any significant relaxant effect on isolated human bronchial smooth muscle [22,23], and, more recently CANDENAS et al [24] have suggested that the 28 amino acid circulating form was also without significant effect. However, our own work has shown that ANP does have a direct relaxant effect in vitro, albeit at relatively high concentrations [25], and that the inhibition of phosphoramidon sensitive protease increases the effect of ANP on airway smooth muscle.…”

Section: Discussionmentioning

confidence: 77%

High dose inhaled atrial natriuretic peptide is a bronchodilator in asthmatic subjects

Hulks¹,

Thomson²

1994

Eur Respir J

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Atrial natriuretic peptide (ANP) has been shown to be an effective bronchodilator when given intravenously, but its efficacy by inhalation has not been assessed.In the first part of the current study, six asthmatic subjects, mean (SEM) forced expiratory volume in one second (FEV 1 ) 2.09 (0.30) l, received 0.1 and 1 mg atrial natriuretic peptide by inhalation, and in the second study five subjects, FEV 1 1.92 (0.40) l, received 5 mg ANP by inhalation. ANP was given in a placebo-controlled, double blind, randomized manner, with measurement of FEV 1 over the following 60 min. Nebulized salbutamol was given at 60 min as a measure of the maximal bronchodilator response attainable by conventional therapy.No significant bronchodilator effect was seen following the 0.1 or 1 mg inhalation, although the latter produced a minimal transient elevation in peripheral atrial natriuretic peptide plasma levels. A bronchodilator effect was seen with the 5 mg dose, which produced ∆FEV 1 0.42 (0.09) l compared to 0.93 (0.13) l subsequently produced by salbutamol. This effect peaked at 5 min and was no different from placebo from 10 min onwards We conclude that atrial natriuretic peptide may produce significant bronchodilation when given by inhalation in high doses, and speculate that substances which generate cyclic guanosine monophosphate (cGMP) in airway smooth muscle warrant further investigation as potential bronchodilatory agents.

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“…ANP and BNP were reported initially to have little relaxant effect on human isolated bronchus, either on basal tone or after stimulation with a contractile agonist [25,35]. However, in later studies ANP produced concentration-dependent, full relaxation of methacholine-contracted human bronchus, with an IC 50 of about 1 µ m [36], and BNP elicited >40% relaxation of non-sensitized sensitized human bronchus contracted with histamine [37].…”

Section: Discussionmentioning

confidence: 99%

“…Recent data link single nucleotide polymorphisms (SNPs) of NPPA, the gene coding for ANP, to asthma susceptibility [21,22]. Furthermore, preclinical in vitro and in vivo studies demonstrate beneficial bronchodilation and anti-inflammatory effects of ANP and BNP [13,15,19,20,23–25]. …”

Section: Introductionmentioning

confidence: 99%

In vitro and in vivo pharmacological profile of PL-3994, a novel cyclic peptide (Hept-cyclo(Cys-His-Phe-d-Ala-Gly-Arg-d-Nle-Asp-Arg-Ile-Ser-Cys)-Tyr-[Arg mimetic]-NH2) natriuretic peptide receptor-A agonist that is resistant to neutral endopeptidase and acts as a bronchodilator

Edelson

Makhlina

Silvester

et al. 2013

Pulmonary Pharmacology & Therapeutics

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The pharmacological and airways relaxant profiles of PL-3994 (Hept-cyclo(Cys-His-Phe-d-Ala-Gly-Arg-dNle-Asp-Arg-Ile-Ser-Cys)-Tyr-[Arg mimetic]-NH2), a novel natriuretic peptide receptor-A (NPR-A) agonist, were evaluated. PL-3994, a full agonist, has high affinity for recombinant human (h), dog, or rat NPR-As (Kis of 1, 41, and 10 nm, respectively), and produced concentration-dependent cGMP generation in human, dog and rat NPR-As (respective EC50s of 2, 3 and 14 nm). PL-3994 has a Ki of 7 nm for hNPR-C but was without effect on cGMP generation in hNPR-B. PL-3994 (1 µm) was without significant effect against 75 diverse molecular targets. PL-3994 or BNP, a natural NPR ligand, produced concentration-dependent relaxation of pre-contracted guinea-pig trachea (IC50s of 42.7 and 10.7 nm, respectively). PL-3994, and also BNP, (0.1 nm–100 µm) elicited a potent, concentration-dependent but small relaxation of pre-contracted human precision-cut lung slices (hPCLS). Intratracheal PL-3994 (1–1000 µg/kg) produced a dose-dependent inhibition of the bronchoconstrictor response evoked by aerosolized methacholine, but was without significant effect on cardiovascular parameters. PL-3994 was resistant to degradation by human neutral endopeptidase (hNEP) (92% remaining after 2 h), whereas the natural ligands, ANP and CNP, were rapidly metabolized (≤1% remaining after 2 h). PL-3994 is a potent, selective NPR agonist, resistant to NEP, with relaxant effects in guinea-pig and human airway smooth muscle systems. PL-3994 has the profile predictive of longer clinical bronchodilator activity than observed previously with ANP, and suggests its potential utility in the treatment of asthma, in addition to being a useful research tool to evaluate NPR biology.

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Effect of atrial natriuretic peptide and on atriopeptins on the human isolated bronchus. Comparison with the reactivity of the guinea-pig isolated trachea

Cited by 16 publications

References 23 publications

Relaxant effect of brain natriuretic peptide in nonsensitized and passively sensitized isolated human bronchi

Relaxant effect of brain natriuretic peptide in nonsensitized and passively sensitized isolated human bronchi

High dose inhaled atrial natriuretic peptide is a bronchodilator in asthmatic subjects

In vitro and in vivo pharmacological profile of PL-3994, a novel cyclic peptide (Hept-cyclo(Cys-His-Phe-d-Ala-Gly-Arg-d-Nle-Asp-Arg-Ile-Ser-Cys)-Tyr-[Arg mimetic]-NH2) natriuretic peptide receptor-A agonist that is resistant to neutral endopeptidase and acts as a bronchodilator

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