Activation of the local renin–angiotensin system (RAS) promotes cardiomyocyte apoptosis and cardiac remodeling after acute myocardial infarction (AMI). As an anti-RAS drug, the effect of Valsartan in the early stage of acute MI is limited by its low drug concentration in the heart and low dosage. Here, by exploiting the inherent nature of neutrophils migrating to the injured myocardium and the local low-pH microenvironment caused by ischemia and hypoxia after myocardial infarction, we designed nanocarrier (NSLP)-hybridized neutrophil membranes and pH-sensitive liposomes (SLPs) for the delivery of Valsartan (NSLP-Val). These functional nanocarriers could mimic neutrophils and are homed to the injured heart; they were also found to respond to a low-pH microenvironment. In the mouse model of MI, we found that NSLP-Val could target the infarct marginal zone and release Valsartan locally in the low-pH microenvironment without affecting hemodynamic stability. Further, locally released angiotensin receptor inhibitors reduced the infarct size and inflammatory response by inhibiting cardiomyocytes. Ultimately, NSLP-Val improved cardiac function and inhibited cardiac hypertrophy and fibrosis.