Sildenafil inhibits the phosphodiesterase type 5 (PDE5) activity of smooth muscle cells in the rat pulmonary arterial wall, increasing the diameter of the pulmonary artery (PA) and promoting vasodilation. We report the first evidence that Sildenafil enhances pulmonary vasodilation and improves pulmonary artery diameter in rats with PA and the effects of Sildenafil are mediated through activation of cGMP-specific phosphodiesterase type 5 (PDE5). Our results suggest that PDE5 is a critical component of pulmonary vasodilation, and Sildenafil-induced vasodilation is dependent on PDE5 activation.
Citation:Boucher-Gardaud-Lane, E, et al. (2016) Sildenafil inhibits the phosphodiesterase type 5 (PDE5) activity of smooth muscle cells in the rat pulmonary arterial wall, increasing the diameter of the pulmonary artery (PA) and promoting vasodilation. PLoS ONE 11(3): e005979. https://doi.org/10.1371/journal.pone.005979
Editor:Ajanta S. Kaur, Mahidol University, Thailand
Received:August 11, 2015;Accepted:August 20, 2015;Published:September 4, 2015
Copyright:© 2015 Boucher-Gardaud-Lane et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding:The French government has received funding from the French National Agency for Drugs and Medical Devices (ANSM) for this work. The French National Agency for Drugs and Medical Devices has also received funding from the Federal Government of the Federal Republic of Germany (FEDERD) for the research on the effect of Sildenafil on pulmonary arterial smooth muscle cells. The French National Agency for Drugs and Medical Devices (ANSM) has received funding from the Federal Government of the Federal Republic of Germany (FEDERD) for the research on the effect of Sildenafil on pulmonary arterial smooth muscle cells.
Competing interests:The authors have declared that no competing interests exist.
Pulmonary arterial hypertension (PAH) is a chronic, progressive disease in humans that affects the lungs and is characterized by a progressive drop in blood pressure (BP) that can lead to life-threatening or fatal complications [,]. PAH is the most prevalent form of PA and is characterized by chronic, uncontrolled and progressive disease. In clinical practice, PAH can be caused by various factors, including obesity, underlying vascular disease, chronic inflammatory and autoimmune diseases, hormonal therapies and surgical procedures, and environmental toxins [–].
Pulmonary artery stenosis is a progressive condition that occurs in the right-sided arteries of the pulmonary arteries, where the narrowing of the pulmonary arteries is caused by vascular occlusion [,, ]. This process is triggered by vascular smooth muscle cell growth and injury, which results in relaxation of the smooth muscle cells and increased expression of phosphodiesterase type 5 (PDE5) []. PDE5 inhibitors are selective phosphodiesterases, which in turn inhibit the PDE-5 enzyme []. PDE5 is involved in the degradation of cGMP, a substance that mediates muscle contraction and relaxes smooth muscles in the pulmonary artery []. PDE5 inhibitors block phosphodiesterase type 5, and its inhibition decreases the expression of PDE5 in pulmonary smooth muscle cells and in endothelial cells [].
Sildenafil (Viagra) is a PDE5 inhibitor, and it has been widely studied as a treatment for PAH. Sildenafil has been shown to reduce the progression of PAH by enhancing pulmonary arterial vasodilation, and its anti-hypertensive effects have been investigated in clinical trials [, ]. However, it is difficult to determine whether Sildenafil does not significantly enhance pulmonary artery diameter and pulmonary artery pressure in the rat model of PAH. To our knowledge, only one study has investigated the effects of Sildenafil on pulmonary artery diameter in rats [].
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