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Effects of hydralazine on the pulmonary vasculature and respiratory control in humans
Author(s) -
Liu Chun,
Balanos George M.,
Fatemian Marzieh,
Smith Thomas G.,
Dorrington Keith L.,
Robbins Peter A.
Publication year - 2008
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2007.039750
Subject(s) - hydralazine , hypoxia (environmental) , blood pressure , medicine , heart rate , pulmonary hypertension , cardiac output , endocrinology , cardiology , chemistry , oxygen , organic chemistry
This study sought: (1) to clarify the effects of hydralazine on both the pulmonary vasculature and respiratory control in euoxia and hypoxia in healthy humans; and (2) to determine whether hydralazine alters the expression of genes regulated by hypoxia‐inducible factor 1 (HIF‐1). Ten volunteers participated in two 2 day protocols. Hydralazine (25 mg) or placebo was administered at 1 pm and 11 pm on the first day, and at 1 pm on the second day. In the mornings and afternoons of both days, we measured plasma vascular endothelial growth factor (VEGF) and erythropoietin (EPO) concentrations (both HIF‐1‐regulated gene products), systemic arterial blood pressure, and changes in heart rate, cardiac output, maximal systolic pressure difference across the tricuspid valve (Δ P max ) and ventilation in response to 20 min of isocapnic hypoxia. Recent hydralazine: (1) decreased diastolic blood pressure; (2) increased heart rate and cardiac output in euoxia and hypoxia whilst having no effect on Δ P max ; and (3) increased the ventilatory sensitivity to hypoxia. Hydralazine had no effect on plasma EPO or VEGF concentration. We conclude that hydralazine increases the sensitivity of the ventilatory response to hypoxia, but lacks any effect on the pulmonary vasculature at the dose studied. It did not affect the expression of HIF‐1‐regulated genes.