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

Cargill, Robert I.; Lipworth, BJ

doi:10.1111/j.1365-2125.1995.tb04528.x

Cited by 37 publications

(20 citation statements)

References 63 publications

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“…In addition to 5-HT, thromboxane, endothelin-1 and angiotensin II, which also bind to G-protein coupled receptors in the pulmonary vasculature [40], have all been reported to cause acute pulmonary arterial vasoconstriction [21,41,42]. In the present study, low doses of the thromboxane receptor agonist U46619 caused an impressive Ppa response in lungs of allergen-sensitised and -challenged mice.…”

Section: Discussionsupporting

confidence: 48%

Allergic lung inflammation induces pulmonary vascular hyperresponsiveness

Witzenrath¹

2006

Eur Respir J

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Pulmonary arterial vasoconstriction is an important early component of pulmonary hypertension. Inflammatory mechanisms play a prominent role in the pathogenesis of pulmonary hypertension. The present authors investigated the potential role of acute allergic lung inflammation for alterations in pulmonary haemodynamics.BALB/c mice were intraperitoneally sensitised to ovalbumin and challenged by ovalbumin inhalation. Subsequently, lungs were ventilated and perfused ex vivo, and pulmonary arterial pressure (Ppa) was continuously monitored.Isolated perfused lungs of allergen-sensitised and -challenged mice showed five-fold enhanced Ppa responses to serotonin, which is reported to be a significant contributor to pulmonary hypertension in humans. This increase in Ppa was abolished by the serotonin receptor-2A antagonist ketanserin, but not the serotonin receptor-1B antagonist GR127935. Intracellular signalling to serotonin involved phosphatidylcholine-specific phospholipase C and protein kinase C, as well as Rho-kinase, as assessed by employing the specific inhibitors D609, bisindolylmaleimide and Y27632, respectively. In addition to serotonin, impressively enhanced Ppa increases in allergic lungs were also evoked by the thromboxane receptor agonist U46619, angiotensin II and endothelin-1.In conclusion, allergic lung inflammation was accompanied by impressive pulmonary vascular hyperresponsiveness. These results suggest a possible role for allergic inflammation in the development of pulmonary arterial hypertension.

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Section: Discussionsupporting

confidence: 48%

Allergic lung inflammation induces pulmonary vascular hyperresponsiveness

Witzenrath¹

2006

Eur Respir J

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“…Activation of RAAS in PAH RAAS has long been recognised to play an important role in pulmonary vascular remodelling and pulmonary vasoconstriction [58,59]. Therefore, when captopril (the first ACE inhibitor) became commercially available, this new drug was eagerly tested in PAH patients, for whom no effective treatment existed at that time.…”

Section: Renin-angiotensin-aldosterone Systemmentioning

confidence: 99%

Perspectives on novel therapeutic strategies for right heart failure in pulmonary arterial hypertension: lessons from the left heart

Handoko

Man

Allaart³

et al. 2010

Eur Respir Rev

111

113

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Right heart function is the main determinant of prognosis in pulmonary arterial hypertension (PAH). At present, no treatments are currently available that directly target the right ventricle, as we will demonstrate in this article.Meta-analysis of clinical trials in PAH revealed that current PAH medication seems to have limited cardiac-specific effects when analysed by the pump-function graph. Driven by the hypothesis that ''left'' and right heart failure might share important underlying pathophysiological mechanisms, we evaluated the clinical potential of left heart failure (LHF) therapies for PAH, based on currently available literature.As in LHF, the sympathetic nervous system and the renin-angiotension-aldosterone system are highly activated in PAH. From LHF we know that intervening in this process, e.g. by angiotensinconverting enzyme inhibition or b-blockade, is beneficial in the long run. Therefore, these medications could be also beneficial in PAH. Furthermore, the incidence of sudden cardiac death in PAH could be reduced by implantable cardioverter-defibrillators. Finally, pilot studies have demonstrated that interventricular dyssynchrony, present at end-stage PAH, responded favourably to cardiac resynchronisation therapy as well.In conclusion, therapies for LHF might be relevant for PAH. However, before they can be implemented in PAH management, safety and efficacy should be evaluated first in well-designed clinical trials.

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“…Since Ang II, through the AT1R receptor, is known to increase intrapulmonary blood pressure and pulmonary vascular resistance, promoting the closure of ductus arteriosus [18,19], we investigated the association between AT1R A 1166 C polymorphism and risk of PDA in 57 premature very low birth weight babies, who were born at less than 29 weeks. We found that the CC genotypecharacterized by increased Ang II-prevents PDA.…”

Section: Introductionmentioning

confidence: 99%

Genetic polymorphisms and risk for acute renal failure in preterm neonates

Vásárhelyi

Tóth-Heyn²,

Treszl

et al. 2004

Pediatr Nephrol

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Acute renal failure (ARF) affects about 10% of severely ill neonates. Recent studies have shown that genetic polymorphisms of proteins that play a role in neonatal physiology may contribute to individual susceptibility to both ARF and its risk factors. Our review summarizes the data collected to date. Studies have shown that the risk of preterm neonates for ARF is directly associated with a combination of high tumor necrosis factor-alpha producer and low interleukin-6 producer genotypes, as well as with low heat shock protein 72 producer genotype. Premature birth is itself the most important risk factor for a number of complications, including ARF, and recent studies have also shown an association between several maternal and fetal cytokine genetic polymorphisms and increased inflammatory response in preterm neonates. These polymorphisms could also be associated with increased risk for disorders such as sepsis and necrotizing enterocolitis, which lead to renal hypoperfusion and ARF. Genetic polymorphisms of the renin-angiotensin-aldosterone system have not been shown to directly influence risk for ARF. They may, however, be associated with patent ductus arteriosus, poor postnatal adaptation, and heart failure, which are all prevalent risk factors for ARF.

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

Cited by 37 publications

References 63 publications

Allergic lung inflammation induces pulmonary vascular hyperresponsiveness

Allergic lung inflammation induces pulmonary vascular hyperresponsiveness

Perspectives on novel therapeutic strategies for right heart failure in pulmonary arterial hypertension: lessons from the left heart

Genetic polymorphisms and risk for acute renal failure in preterm neonates

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