Nitric Oxide and Other Novel Therapies for Pulmonary Hypertension

Claudio Napoli, Joseph Loscalzo

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Pulmonary hypertension is an uncommon, yet devastating, syndrome with a complex underlying pathobiology. Hypoxia, inflammation, and increased shear stress appear to be the primary pathogenic events; however, mechanisms by which these processes lead to pulmonary hypertension remain incompletely understood. The ultimate increase in pulmonary vascular resistance is attributed to remodelling of the walls of resistance vessels, which can lead to encroachment on and reduction of the vascular lumen. The number of blood vessels per unit of cross-sectional area in the hypertensive lung is also reduced, which can contribute to increased vascular resistance. Regardless of its etiology, endothelial dysfunction underlies pulmonary hypertension, one manifestation of which is the attenuated production of bioactive nitric oxide. Nitric oxide administration can exert beneficial effects at various stages of the disease. Here we review the known pathobiology of pulmonary hypertension, with a principal focus on endothelial nitric oxide, and also summarize the data on nitric oxide replacement therapy and other novel therapies that relate to nitric oxide as one approach to treatment.

Original languageEnglish
Pages (from-to)1-8
Number of pages8
JournalJournal of Cardiovascular Pharmacology and Therapeutics
Volume9
Issue number1
Publication statusPublished - Mar 2004

Fingerprint

Pulmonary Hypertension
Nitric Oxide
Vascular Resistance
Blood Vessels
Therapeutics
Inflammation
Lung

Keywords

  • Endothelial cell
  • Hypoxia
  • Primary pulmonary hypertension

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Nitric Oxide and Other Novel Therapies for Pulmonary Hypertension. / Napoli, Claudio; Loscalzo, Joseph.

In: Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 9, No. 1, 03.2004, p. 1-8.

Research output: Contribution to journalArticle

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