Since activation of GPR91 in kidney can increase blood pressure through the renin-angiotensin system (RAS) [11], the question remained whether cardiac hypertrophy, induced by high levels of succinate in the blood stream, was a consequence of succinate-induced changes in mean arterial blood pressure (MAP) through RAS activation, rather than a direct effect of succinate through GPR91 in the heart. This evidence concerns the gene SUCNR1 and cardiac hypertrophy.