The involvement of Rho-kinase (ROCK) in VEGF-driven endothelial migration and angiogenesis has been implied, and current studies address ROCK-inhibition as a potential therapeutic target after myocardial infarction (MI). However, ROCK-inhibitors also interfere with contractile processes and potentially blunt the early compensatory phase after MI. Hence, neurohumoral activation of CNS and RAAS in the early phase after MI is thought to help maintain cardiac output and organ perfusion. The present study investigated the effect of H-1152 on vascular contractility shortly after MI. Normal Wistar rats were subjected either to sham-surgery, MI-surgery or MI-surgery plus treatment with the ROCK-inhibitor H-1152 started immediately after surgery. One week following surgery rats were sacrificed, the aorta removed and studied in vitro for contractile responses to phenylephrine (PE) and angiotensin II (AngII). Contractile responses both to PE and AngII were profoundly increased in untreated MI, as compared to untreated sham rats. Presence of the eNOS-inhibitor L-NMMA increased and fully abolished the differences in PE-responses, thus suggesting reduced basal release of NO to inhibit contractility in MI-rats. Although presence of L-NMMA also increased responses to AngII in sham and MI, maximal contraction remained increased in the latter. Interestingly, pre-incubation with AG 1478 – an EGF-receptor inhibitor – reduced contractile responses to AngII in MI, but not sham. The latter finding is suggestive for increased involvement of AT1-EGR receptor transactivation following MI. Finally, PE- and AngII-induced responses did not differ between MI rats treated or without H-1152. Increased contractility to PE and AngII following MI involved reduced basal release of NO and possibly increased AT1-EGF-receptor transactivation. Treatment with the ROCK-inhibitor H-1152 did not adversely affect these adaptations in contractility following MI.