Effects of continuous infusion of atrial natriuretic peptide on the pulmonary hypertension induced by chronic hypoxia in rats

Zhao, Lan; Winter, R. J. D.; Krausz, Thomas; Hughes, J. M. B.

doi:10.1042/cs0810379

Cited by 31 publications

(21 citation statements)

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“…In an animal model, as well as blunting acute HPV, ANP has also been shown to attenuate the development of pulmonary hypertension and pulmonary vascular remodelling [18]. BNP has not been studied with respect to attenuation of acute or chronic pulmonary vascular responses to hypoxaemia.…”

Section: Discussionmentioning

confidence: 99%

Acute effects of ANP and BNP on hypoxic pulmonary vasoconstriction in humans.

Cargill

Lipworth

1995

Brit J Clinical Pharma

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1 Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) have pulmonary vasorelaxant activity with plasma concentrations being elevated in patients with hypoxaemic pulmonary hypertension. However, their effects on acute hypoxic pulmonary vasoconstriction (HPV), the initiating stimulus for pulmonary hypertension have not to date been investigated. We have therefore studied the effects of ANP and BNP on acute HPV in humans. 2 Eight healthy volunteers were studied on three separate occasions. After reaching a resting haemodynamic state (to), an infusion of either ANP (10 pmol kg-1 min-'), BNP (10 pmol kg-1 min-1) or placebo (5% dextrose) was commenced. This was given alone for 30 min (t30) before subjects were rendered hypoxaemic (SaO2 75-80%) for a further 30 min (t60), with the initial infusion continuing to t60. Pulsed-wave Doppler analysis of pulmonary artery flow was used to measure mean pulmonary arterial pressure (MPAP) and hence total pulmonary vascular resistance (PVR) was calculated. Keywords natriuretic peptides hypoxaemia pulmonary circulation Introduction remains unknown but the beneficial effects of lung blood flow redistribution are more clear. Vasoconstriction in The vasoconstriction of the mammalian pulmonary areas of alveolar hypoxia leads to diversion of blood vasculature in response to hypoxia has intrigued physiol-flow away from hypoxic regions hence improving overall ogists since the phenomenon was first described by Von ventilation/perfusion matching [2]. This response can, Euler & Liljestrand [ 1]. The exact mechanism under-however, be detrimental if hypoxia is chronic and affects lying acute hypoxic pulmonary vasoconstriction (HPV) the whole lung, as is seen in hypoxaemic chronic

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Section: Discussionmentioning

confidence: 99%

Acute effects of ANP and BNP on hypoxic pulmonary vasoconstriction in humans.

Cargill

Lipworth

1995

Brit J Clinical Pharma

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“…In vivo, ANP attenuates the acute vasoconstrictor response to hypoxia in pigs [53]. In addition to these acute effects, ANP has been shown to prevent the pulmonary vascular remodelling seen in response to chronic hypoxia in rats [60].…”

Section: Interaction With Hypoxaemiamentioning

confidence: 99%

The role of the renin‐angiotensin and natriuretic peptide systems in the pulmonary vasculature.

Cargill

Lipworth

1995

Brit J Clinical Pharma

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1 The role of vasoactive peptide systems in the pulmonary vasculature has been studied much less extensively than systemic vascular and endocrine effects. The current understanding of the role of the renin-angiotensin (RAS) and natriuretic peptide systems (NPS) in the pulmonary ciruclation is therefore reviewed. 2 Plasma concentrations of angiotensin II, the main vasoactive component of the RAS, are elevated in pulmonary hypertension and may interact with hypoxaemia to cause further pulmonary vasoconstriction. Pharmacological manipulation of angiotensin II can attenuate hypoxic pulmonary vasoconstriction but larger studies are needed to establish the efficacy of this therapeutic strategy in established pulmonary hypertension. 3 Although all the known natriuretic peptides, ANP, BNP and CNP are elevated in cor pulmonale, only ANP and BNP appear to have pulmonary vasorelaxant activity in humans. ANP and BNP can also attenuate hypoxic pulmonary vasoconstriction, suggesting a possible counter-regulatory role for these peptides. Inhibition of ANP/BNP metabolism by neutral endopeptidase has been shown to attenuate development of hypoxic pulmonary hypertension but this property has not been tested in humans. 4 It is also well established that there are potentially important endocrine and systemic circulatory interactions between the RAS and NPS. This also occurs in the pulmonary circulation and in humans, where at least BNP acts to attenuate angiotensin II induced pulmonary vasoconstriction. This interaction may be particularly relevant as a mechanism to counter-regulate overactivity of the RAS. 5 Although the NPS and RAS have profound effects on the pulmonary circulation, the therapeutic potential of manipulating these systems has yet to be realised.

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“…Nitric oxide (NO) and the natriuretic peptides attenuate vasoconstriction and vascular remodeling in hypoxia-induced pulmonary hypertension 4,5 but are difficult to administer as drugs over the long term. Their vasorelaxant and antimitogenic actions are mediated by cGMP and activation of cGMPdependent protein kinases.…”

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confidence: 99%

Sildenafil Inhibits Hypoxia-Induced Pulmonary Hypertension

Zhao

Mason²,

Morrell³

et al. 2001

Circulation

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Background-This study investigated the effect of the phosphodiesterase 5 inhibitor sildenafil on the pulmonary vascular response to hypoxia in humans and mice. Methods and Results-In a randomized, double-blind study, sildenafil 100 mg or placebo was given orally to 10 healthy volunteers 1 hour before breathing 11% O 2 for 30 minutes. Pulmonary artery pressure (PAP) was measured with an indwelling right heart catheter.

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Effects of continuous infusion of atrial natriuretic peptide on the pulmonary hypertension induced by chronic hypoxia in rats

Cited by 31 publications

References 0 publications

Acute effects of ANP and BNP on hypoxic pulmonary vasoconstriction in humans.

Acute effects of ANP and BNP on hypoxic pulmonary vasoconstriction in humans.

The role of the renin‐angiotensin and natriuretic peptide systems in the pulmonary vasculature.

Sildenafil Inhibits Hypoxia-Induced Pulmonary Hypertension

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