TRPV1 Receptor Stimulates Myocardial Protection in Hypertensive Rats Through Regulation of Mitochondrial Function

The TRPV1 receptor is expressed on various cell types, including cardiomyocytes. Activation of TRPV1 leads to regulation of Ca²⁺ flux across both cell and mitochondrial membranes, which could control the ion flux under experimental systemic arterial hypertension (SAH), particularly in mitochondria, and thus prevent heart damage. In this study, SAH was induced in male Wistar rats using L-NAME, providing a system in which the regulatory action of nitric oxide (NO) is inhibited. The animals were divided into five groups: 1) Control (C), 2) Hypertensive (H), 3) H+Capsaicin (H+CS), 4) H+Capsazepine (H+CZ), and 5) H+CS+CZ. L-NAME was added to drinking water at a concentration of 200 mg/L for 40 days. Four days before the end of the L-NAME treatment, a daily subcutaneous dose of CS (5 mg/kg in the H+CS group), CZ (6 mg/kg in the H+CZ group), or a combination of CS+CZ was administered. We analyzed mitochondrial function and the damage caused by hypertension in the heart. The activation of TRPV1 under SAH conditions improved mitochondrial respiratory control, regulated oxidative stress, and modulated pro-apoptotic proteins. The improvement in mitochondrial metabolism led to the prevention of damage and better heart function.