Hydrogen Sulfide Increases Excitation-Contraction Coupling Efficiency and Modulates LCC and SERCA2a Function in Hypertensive Rats
8 de febrero 2024
Te invitamos a leer el artículo: "Hydrogen Sulfide Increases Excitation-Contraction Coupling Efficiency and Modulates LCC and SERCA2a Function in Hypertensive Rats", realizado por la Dra. Norma Viquez y el Dr. David Centurión, investigadores de la Sede Sur del Cinvestav.
Autores: Grecia J. Medina Terol , Luis F. Chimal Ávila , Maritza Mayorga Luna , Karla Carvajal , David Centurión y Norma L. Gómez Viquez.
Abstrac: Hypertension-induced cardiac hypertrophy (HICH) leads to alterations in excitation-contraction coupling (ECC) by modifying the function of proteins involved in this process, such as the sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) and L-type Ca2+ channel (LCC). Hydrogen sulfide (H2S) is a gasotransmitter that protects the heart against HICH, but it remains unknown whether its cardioprotective action is related to an improvement in the ECC. We evaluated the effects of chronic administration of NaHS, a H2S donator, on ECC efficiency and SERCA2a and LCC function in rats with abdominal aortic coarctation (AAC). ECC was assessed by recording the Ca2+ transients (CaT) induced by electrical stimulation in isolated ventricular myocytes. Properties of ECC were evaluated by determining amplitude (ΔCa2+), sarcoplasmic reticulum (SR) Ca2+ release velocity (dCa/dtmax), time to peak (Tp), and efficiency of ECC (dCa/dt/ΔCa2+) during the rising phase of CaT. SERCA2a activity was evaluated by measuring the time constant (τ) of CaT decay phase. SR Ca2+ load was determined by applying a caffeine pulse at the end of electrical stimulation. SERCA2a and LCC expression were assessed by western blot. Data were presented as mean ± S.E.M and were evaluated using one-way ANOVA followed by a Tukey posthoc test. AAC decreased ΔCa2+, dCa/dtmax, dCa/dt/ΔCa2+ and SR Ca2+ load but didn't change τ. Moreover, AAC increased LCC expression but didn’t modify SERCA2a and PLB expression. Treatment with 5.6 mg/kg NaHS didn’t restore ΔCa2+, dCa/dtmax or SR Ca2+ load, but reestablished dCa/dt/ΔCa2+ and LCC expression. Additionally, NaHS decreased τ. These results suggest that cardioprotective role of H2S during HICH is related to an increase in SERCA2a activity and ECC efficiency.