Hence compensatory hyperinsulinemia in IR can lead to enhanced sodium reabsorption resulting in HT.14 Similarly, activation of the RAS results in increased angiotensin II (AT-II), which is a potent vasoconstrictor; AT-II inhibits differentiation of adipocytes, thereby causing IR and mitochondrial dysfunction.15 Angiotensin II inhibits the phosphatidyl inositol-3 kinase pathway, thereby affecting downstream insulin-mediated actions. This evidence concerns the gene INS and hyperinsulinism.