enhance these protective effects in the hearts of diabetic rats. Chronic Resveratrol treatment with Ipost neither reduced infarct size nor increased myocardial dysfunction recovery in both diabetic and non-diabetic rats (infarct size: 59.5% and 59.2% in diabetic ones and 45.0% and 43.7% in non-diabetic ones, P>0.05, respectively), and this might be associated with an inhibition of Akt and eNOS phosphorylation. Conclusions: The combination of acute Resveratrol treatment with Ipost shows a stronger protective effect within the hearts of diabetic rats, but chronic Resveratrol with Ipost fails to protect hearts against reperfusion injury in either diabetic or nondiabetic rat hearts. These findings will be important for the design of future clinical investigations.Objectives: Our studies demonstrate that deletion of the transient receptor potential vanilloid type 1 (TRPV1) gene aggravates deoxycorticosterone acetate (DOCA) -salt hypertension-induced renal injury, which is associated with increased intra-renal monocyte/macrophage infiltration and inflammation. The results suggest that TRPV1 may act as a potential regulator of monocyte/macrophage infiltration to reduce renal injury in DOCA-salt hypertension. Therefore, this study was designed to test the hypothesis that deletion of TRPV1 exaggerates salt-sensitive hypertension-induced renal injury via activation of chemokine receptor 2 (CCR2). Methods: We induced salt-sensitive hypertension for 4 weeks by uninephrectomy and DOCA-salt in wild type (WT) and TRPV1-null mutant (TRPV1 -/-) mice with or without the selective CCR2 antagonist, RS504393. Results: DOCA-salt treatment increased systolic blood pressure (SBP) to the same degree in both strains, but increased urinary excretion of albumin and 8-isoprostane and decreased creatinine clearance with greater magnitude in TRPV1 -/mice