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Abstract
Increased pulmonary vascular resistance and smooth muscle hypertrophy characterize pulmonary hypertension (PAH). Only a few downstream mediators can induce such changes among these being altered Ca++ signaling. A family of ion channels, the transient receptor potential proteins (TrpCs), has been identified that activate Ca++ flux and affect cell function. Thus we tested the hypothesis that PAH induces specific TrpCs.
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