This afferent arteriolar dilation can be attributed to increased prostaglandin E2 synthesis, impaired responsiveness to vasoconstrictors (i.e., thromboxane and norepinephrine), elevated levels of atrial natriuretic peptide (ANP), and hyperglycemia-mediated inactivation of tubuloglomerular feedback (TGF) [182]. The gene discussed is NPPA; the disease is Hyperglycemia.