Nitric oxide released from endothelial cells causes vasodilation of vascular smooth muscle. Downstream of soluble guanylyl cyclase activation, what is the principal effector mechanism?
- A cGMP-dependent protein kinase phosphorylates targets that lower cytosolic calcium and increase myosin light chain phosphatase activity ✓
- B cGMP directly chelates calcium released from the sarcoplasmic reticulum
- C Nitric oxide nitrosylates myosin light chain kinase at its calmodulin-binding domain
- D cGMP opens plasmalemmal calcium channels, raising calcium to trigger repolarization
Correct answer: A. cGMP-dependent protein kinase phosphorylates targets that lower cytosolic calcium and increase myosin light chain phosphatase activity
Explanation
NO diffuses into the smooth muscle cell and activates soluble guanylyl cyclase, raising cGMP. Protein kinase G then reduces intracellular free calcium by increasing uptake into stores and decreasing entry, and it promotes dephosphorylation of MLC20 through phosphatase activation, so cross-bridge cycling falls and the vessel dilates. Sildenafil potentiates this pathway by inhibiting cGMP breakdown, a fact that confirms PKG rather than direct calcium chelation as the effector step.
Reference: Ganong's Review of Medical Physiology, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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