Decreased Expression of Transient Receptor Potential Vanilloid 1 Impaires the Postischemic Recovery of Diabetic Mouse Hearts

BACKGROUND: We hypothesized that the transient receptor potential vanilloid type 1 (TRPV1), which is found in the sensory nerve fibers, could modulate the cardiac function, be impaired by diabetes and could contribute to further severe postischemic heart injury. METHODS AND RESULTS: Diabetes was induced in ICR mice by an intraperitoneal injection of streptozotocin. The expression of both TRPV1 and calcitonin gene-related peptide (CGRP) in diabetes mellitus (DM) hearts was significantly lower, as determined by Western blot and radioimmunoassay, respectively. During the ischemia/reperfusion, the cardiac function was measured by a Medlab system and the lactate dehydrogenase (LDH) in the effluents was measured by an ELISA kit. Compared with the non-DM hearts, the DM hearts demonstrated increased left ventricular end-diastolic pressure and decreased left ventricular developed pressure, heart rate and coronary flow, and also released more LDH in the effluents. Pretreatment with capsaicin attenuated the postischemic injury significantly in non-DM hearts, but not in DM hearts. Pretreatment with CGRP in both non-DM and DM hearts protected hearts against ischemic injury. CONCLUSIONS: The alteration of TRPV1 caused by diabetes is related to the poor recovery of cardiac function after myocardial ischemia.