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. 2014 Nov 26;12:314. doi: 10.1186/s12967-014-0314-y

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© Cavasin et al.; licensee BioMed Central Ltd. 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Monotherapy to block PDE-5 or ET _A signaling modestly reduces pulmonary pressure and RV hypertrophy. (A) Study design. Animals received 10 mg/kg tadalafil (TAD) or ambrisentan (AMB) once daily by oral gavage starting after week three. (B–C) Mean pulmonary arterial pressure (mPAP) and PA pulse pressure (PAPP) were measured invasively at study endpoint. (D) RV hypertrophy was assessed by weighing ventricular chambers at the time of necropsy, and is expressed as a ratio to LV + septum (S). (E) The gene encoding regulator of calcineurin-1 (RCAN1) is regulated by the nuclear factor of activated T cells (NFAT) transcription factor, which translocates to the nucleus in response to dephosphorylation by the pro-hypertrophic phosphatase, calcineurin. (F) RCAN1 expression in RV homogenates was detected by immunoblotting. Calnexin served as a loading control. Values represent mean +/−SEM. *P < 0.05 vs. normoxia; ^† P < 0.05 vs. SU-Hx + vehicle (Veh). AMB significantly reduced pulmonary arterial pressure and RV hypertrophy, while TAD was without effect. Neither compound consistently blocked RV calcineurin signaling.