Abstract
A small GTPase RhoA and its downstream effectors Rho-associated protein kinases (ROCK) signaling pathway activation mediate smooth muscle contraction. ROCKs inhibit myosin light chain phosphatase (MLCP) dephosphorylation and therefore reduce relaxation. However, nitric oxide (NO) that is produced and released from endothelial cells has an inhibitory effect on the ROCK pathway in vasculature. Studies in which ROCK activity was inhibited by variety of pharmacological agents (HA1077 or Y-27632) have shown that it has some critical effects on systemic diseases like hypertension or diabetes mellitus. Indeed this activity may show isoform specificity (ROCK1 or ROCK2) dependent on the pathology. Therefore, in vascular pathogenesis ROCK pathway with its isoforms also need to be considered due to its direct effects on the vasoconstriction.
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