Step 1: Identify the pathway. Nitric oxide is the classic endothelium-derived relaxing factor, so we expect a second-messenger answer linked to vasodilation.
Step 2: NO binds the haem group of soluble guanylate cyclase. This enzyme then makes $cGMP$ from $GTP$, so the immediate measurable effect of NO is a jump in cellular $cGMP$.
Step 3: Elevated $cGMP$ drives protein kinase G, reduces cytosolic calcium and relaxes vascular smooth muscle. This explains why nitrates and PDE-5 inhibitors (which preserve cGMP) cause vasodilation.
Step 4: Eliminate the rest - BRCA1 and BRCA2 are DNA-repair genes tied to breast and ovarian cancer, and interleukins are immune messengers; none are downstream of NO. The signalling molecule increased is cyclic GMP.\[\boxed{cGMP}\]