An intravenous dose of epinephrine produces hepatic glycogenolysis and intestinal smooth muscle relaxation in one patient, while producing marked splanchnic vasoconstriction in another experimental setting. The biochemical explanation for these opposing responses in different tissues is:

• A Epinephrine is metabolized differently by MAO versus COMT in various organs
• B Hepatic cells convert epinephrine to norepinephrine before responding
• C Epinephrine concentration determines whether it crosses the blood-brain barrier
• D Different tissues express different adrenergic receptor subtypes coupled to distinct G proteins ✓

Explanation

Receptor subtype distribution dictates the response. Hepatic beta2 receptors couple to Gs and raise cAMP for glycogenolysis, whereas splanchnic vascular alpha1 receptors couple to Gq, activating PLC, IP3, calcium release, and contraction. The same ligand gives opposite physiological outcomes purely based on receptor-G protein coupling. Options A and B invoke metabolism changes that do not occur, since circulating epinephrine acts as an intact hormone, and COMT or MAO only degrades it after uptake.

Reference: Ganong's Review of Medical Physiology, 26th ed.

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