In early hypertension, nNOS-derived NO is involved in increases of cGMP/PKG-dependent troponin I (TnI-Ser(23/24)) and cardiac myosin binding protein C (cMBP-C-Ser(273)).
In this way, a drug that we termed G1 was identified, which targets C42 of PKG Iα to induce vasodilation of isolated resistance blood vessels and blood pressure lowering in a mouse model of angiotensin II-induced hypertension.
Multiple logistic regression adjusted for age and sex showed that subjects carrying rs7897633-A (PRKG1), rs434082-A (SLC8A1) and rs1042714-G (ADRB2) risk alleles had 1.83-, 2.84- and 2.40-fold increased risk for salt-sensitive hypertension, respectively.
Thus, the NF-κB/miR-155-5p/PKG1 axis may be crucial in the pathogenesis of inflammatory vascular diseases, such as atherosclerotic intimal hyperplasia and preeclamptic hypertension.