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Fig. 2 | Clinical Hypertension

Fig. 2

From: Neuronal nitric oxide synthase in hypertension – an update

Fig. 2

Schematic diagram of nNOS up-regulation by Ang II in cardiac myocytes and the potential target proteins, mechanism of regulation in cardiac myocytes from hypertension. Left. Ang II stimulates AT1R and NADPH oxidase in cardiac myocytes. AT1R and intracellular ROS activates Akt and phosphorylates endogeneous eNOS to produce NO. eNOS and NO-dependent S-nitrosation of AT2R lead to the translocation of AT2R to the plasma membrane and induces nNOS protein and increases NO production (data modified from Figure 8 of Basic Research in Cardiology, 2015, 110 (3):21). In hypertension, cardiac nNOS is up-regulated and facilitates myocyte relaxation. nNOS reduces Ca2+ influx via LTCC and promotes Ca2+ re-uptake via SERCA through PLN phosphorylation (secondary to PPase-dependent PKA phosphorylation) in healthy heart. In hypertension, nNOS inhibits LTCC and phosphorylates cMBP-C Ser273 and cTnI Ser23/24 via cGMP/PKG-dependent mechanism. As a result, myofilament Ca2+ sensitivity is reduced which accounts for nNOS-dependent positive lusitropy in hypertension

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