NBME 16 Question - joeyramonesghost

[ArchivalUser]

A 66-year-old man is brought to the emergency department 30 minutes after the sudden onset of substernal chest pain that radiates to the neck and left arm; the pain is associated with weakness, nausea, and profuse sweating. He was jogging during the onset of pain. He has a 5-year history of hypertension treated with indapamide. His pulse is 90/min, and blood pressure is 150/90 mm Hg. Cardiac examination shows an S4. Treatment with a sublingual medication resolves his pain within 2 minutes. Which of the following mechanisms of action of the drug most likely led to the relaxation of vascular smooth muscle in this patient?

A) Decreasing intracellular calcium
B) Increasing cAMP
C) Increasing cGMP
D) Inhibiting the sodium pump
E) Stabilizing depolarization of the vascular smooth muscle membrane

[ArchivalUser]

It seems clear that the drug in question is an NO donator of some kind. My confusion lies here: it's my understanding that NO dilates vascular smooth muscle by an increase in cGMP *and* a subsequent decrease in intracellular calcium.

I chose A and it was incorrect. Help me understand.

[ArchivalUser]

CC the increase in cGMP is direct effect

[ArchivalUser]

Ahh.. "direct effect" I see. So the calcium drop is the effect of cGMP not directly NO. Thanks.

[ArchivalUser]

CC

"Nitroglycerin" get converted into "Nitric Oxide"(NO)

NO --> + Guanylate Cyclase ( that convert GTP into cGMP) --> "Increased cGMP" ---> + PKG


Protein Kinase G ---> + MLC-Phosphatase ----> Dephosphoration of Myosin Light Chain (MLC)

*A Dephosphorylated MLC is unable to interact with ACTIN ----> "RELAXATION"


NOTE: Diagram on Page 418 FA 2014