Dec. 26, 2009 Blood pressure is controlled in part by changes in the radius of blood vessels; when the smooth muscle cells in the wall of a blood vessel contract, the radius of the blood vessel decreases and blood pressure increases.
A team of researchers at CSIC-University of Salamanca, Spain, has now identified in mice a new signaling pathway that contributes to relaxation of smooth muscle cells in blood vessel walls triggered by the molecule NO and thereby decreases blood pressure.
Mice lacking the protein Vav2 have elevated blood pressure. By analyzing these mice, the team, led by Xosé Bustelo, identified a Vav2 signaling pathway that normally contributes to NO-triggered relaxation of smooth muscle cells in blood vessel walls. The pathway involves Vav2 activation of the proteins Rac1 and Pak1. Absence of Pak1 activation in Vav2-deficient mice resulted in excessive activity of the protein phosphodiesterase type 5. Consistent with this, treating Vav2-deficient mice with phosphodiesterase type 5 inhibitors reduced their blood pressure to a normal level.
As defective blood vessel reactivity to NO contributes to the symptoms of diseases such as atherosclerosis (hardening of the arteries) and diabetes, the authors suggest that stimulating the pathway they have identified might be of therapeutic benefit in patients with these diseases.
The research is reported in the Journal of Clinical Investigation.
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- Vincent Sauzeau, María A. Sevilla, María J. Montero, and Xosé R. Bustelo. The Rho/Rac exchange factor Vav2 controls nitric oxide-dependent responses in mouse vascular smooth muscle cells. Journal of Clinical Investigation, 2009; DOI: 10.1172/JCI38356
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