A 58-year-old man with type 2 diabetes reports inability to achieve an erection adequate for intercourse, though nocturnal erections were previously normal. Penile tumescence depends primarily on which mediator released from parasympathetic nerve endings and endothelium?
- A Nitric oxide increasing cyclic GMP in corporal smooth muscle ✓
- B Noradrenaline acting on alpha-1 receptors
- C Acetylcholine acting on nicotinic receptors of the helicine arteries
- D Prostaglandin E1 increasing intracellular calcium
Explanation
Erection is a parasympathetic event mediated by nitric oxide, which activates guanylyl cyclase, raises cyclic GMP and relaxes smooth muscle in the corpora cavernosa and helicine arteries, allowing lacunar filling. Diabetes causes autonomic neuropathy and endothelial dysfunction, reducing NO availability. Noradrenaline mediates detumescence via alpha-1 receptors, so option B produces the opposite effect. Intracellular calcium rise causes contraction, not relaxation, ruling out D, and nicotinic receptors are ganglionic rather than the effector target here.
Reference: Ganong's Review of Medical Physiology, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.