Researchers found that treatments with MLT and ACE2 inhibitors could relieve the pathological changes observed in rats exposed to prolonged light exposure, including HTN, enlargement of the left ventricle, and hardening of the left ventricle and aorta, along with increased oxidative stress.[45] Additionally, both the release and circulating levels of MLT are diminished in patients with both acute and chronic HF.[46] Importantly, blood MLT levels show an inverse relationship with N-terminal pro-brain natriuretic peptide levels, which is a marker associated with HF.[9,20]. The gene discussed is ACE2; the disease is hydrops fetalis.