Sildenafil for the Treatment of Pulmonary Hypertension in Pediatric Patients

Huddleston, Alice J.; Knoderer, Chad A.; Morris, Jennifer; Ebenroth, Eric S.

doi:10.1007/s00246-009-9523-1

Cited by 54 publications

(45 citation statements)

References 76 publications

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“…The mechanism underlying this effect might be through suppression of calcium influx by PKG to decrease intracellular calcium (Fiedler et al, 2002). Sildenafil has been recently shown to be an important medicine in the clinic treatment of pulmonary hypertension (Anderson and Nawarskas, 2010;Chapman et al, 2009;Huddleston et al, 2009); our study adds a novel insight to the effects of sildenafil in the treatment of pulmonary hypertension.…”

Section: Discussionmentioning

confidence: 80%

Sildenafil inhibits calcineurin/NFATc2-mediated cyclin A expression in pulmonary artery smooth muscle cells

Liu

Sun

et al. 2011

Life Sciences

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Section: Discussionmentioning

confidence: 80%

Sildenafil inhibits calcineurin/NFATc2-mediated cyclin A expression in pulmonary artery smooth muscle cells

Liu

Sun

et al. 2011

Life Sciences

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“…There is no effect of sildenafil on normal cardiac function in WT controls. (66), but some patients are unresponsive to iNO, or it can be difficult to wean them from dependency on the drug (165,201). Evidence suggests that PDE activities impact pulmonary vascular tone in infants and changes following hyperoxic damage (62,87,100,270,329,412).…”

Section: Expanded Uses For Approved Pde5 Inhibitorsmentioning

confidence: 99%

Mammalian Cyclic Nucleotide Phosphodiesterases: Molecular Mechanisms and Physiological Functions

Francis

Blount

Corbin

2011

Physiological Reviews

560

546

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The superfamily of cyclic nucleotide (cN) phosphodiesterases (PDEs) is comprised of 11 families of enzymes. PDEs break down cAMP and/or cGMP and are major determinants of cellular cN levels and, consequently, the actions of cN-signaling pathways. PDEs exhibit a range of catalytic efficiencies for breakdown of cAMP and/or cGMP and are regulated by myriad processes including phosphorylation, cN binding to allosteric GAF domains, changes in expression levels, interaction with regulatory or anchoring proteins, and reversible translocation among subcellular compartments. Selective PDE inhibitors are currently in clinical use for treatment of erectile dysfunction, pulmonary hypertension, intermittent claudication, and chronic pulmonary obstructive disease; many new inhibitors are being developed for treatment of these and other maladies. Recently reported x-ray crystallographic structures have defined features that provide for specificity for cAMP or cGMP in PDE catalytic sites or their GAF domains, as well as mechanisms involved in catalysis, oligomerization, autoinhibition, and interactions with inhibitors. In addition, major advances have been made in understanding the physiological impact and the biochemical basis for selective localization and/or recruitment of specific PDE isoenzymes to particular subcellular compartments. The many recent advances in understanding PDE structures, functions, and physiological actions are discussed in this review.

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“…Sildenafil can ameliorate erectile dysfunction in elderly men, but had a lower efficacy rate with increasing age (Muller et al, 2007). Moreover, this drug showed an efficacy in treatment of pulmonary hypertension in children and in patients with hemoglobinopathies that lead to severe pulmonary hypertension (Huddleston et al, 2009). Some studies have provided promising evidences that sildenafil can be used as tolerated treatment option for benign prostatic hyperplasia (Wang et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Propolis Protective Role Against Morphological, Hormonal Biochemical and Histological Alterations Induced by Sildenafil Overdoses

Al‐Μansour

Jarrar

2016

Int. J. Morphol.

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Sildenafil for the Treatment of Pulmonary Hypertension in Pediatric Patients

Cited by 54 publications

References 76 publications

Sildenafil inhibits calcineurin/NFATc2-mediated cyclin A expression in pulmonary artery smooth muscle cells

Sildenafil inhibits calcineurin/NFATc2-mediated cyclin A expression in pulmonary artery smooth muscle cells

Mammalian Cyclic Nucleotide Phosphodiesterases: Molecular Mechanisms and Physiological Functions

Propolis Protective Role Against Morphological, Hormonal Biochemical and Histological Alterations Induced by Sildenafil Overdoses

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