A 55-year-old diabetic man is prescribed prazosin for hypertension. He develops orthostatic hypotension on standing. The normal reflex that prazosin disrupts is mediated by:
- A Beta-2 adrenoceptor mediated venous constriction on standing
- B Muscarinic cholinergic constriction of capacitance vessels
- C Neuropeptide Y mediated vasoconstriction independent of adrenergic receptors
- D Alpha-1 adrenoceptor mediated arteriolar and venous constriction in response to baroreceptor-triggered sympathetic activation on standing ✓
Explanation
On standing, gravitational pooling of blood in dependent veins reduces venous return and cardiac output, causing a transient drop in arterial pressure sensed by baroreceptors (carotid sinus, aortic arch). Baroreceptor unloading increases sympathetic outflow and reduces parasympathetic tone. Sympathetic norepinephrine acts on alpha-1 adrenoceptors in arterioles (increasing TPR) and veins (increasing venous return via venoconstriction), restoring blood pressure within seconds. Prazosin, an alpha-1 blocker, prevents this compensatory vasoconstriction, causing orthostatic hypotension. Beta-2 receptors mediate vasodilation in skeletal muscle and bronchodilation; muscarinic receptors do not mediate vasoconstriction; NPY contributes but is not the primary acute reflex mediator.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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