Pulmonary arterial hypertension (PAH) results in right ventricular failure due to markedly elevated pulmonary arterial pressure and compensatory right ventricular hypertrophy. Although the involvement of tyrosine kinase (PTK) in the smooth muscle pathogenicities of PAH has been suggested, attempts to treat with a “multi-target” PTK inhibitor (PTKI) have not made sufficient progress due to harmful effects such as cardiotoxicity. In this study, we searched for PTK, whose expression is selectively increased in the hypertrophied right ventricular wall of PAH rats. RT-PCR targeting PTK domain consensus sequence was carried out for right ventricular wall (RV) and left ventricular wall with septum (LV+S) from monocrotaline-induced (MCT-) PAH rats and control rats. Southern hybridization was performed using various PTK probes derived from MCT-PAH rat RV. Selective increased expression of at least three types of PTK in MCT-PAH rat RV was observed, including PDGF-Rβ, which we previously reported its overexpression in pulmonary arteries of MCT-PAH rats. There was no difference in the expression of c-abl, which is thought to be involved in PTKI cardiotoxicity, in the LV+S and RV in both PAH and control rats. Our results suggest that a more specific inhibition of PTK isoform would be suitable for safely treating PAH using PTKI.