## α1-Adrenergic Receptors and Vasoconstriction **Key Point:** α1-adrenergic receptors on vascular smooth muscle mediate vasoconstriction when activated by noradrenaline or adrenaline released from sympathetic terminals. **High-Yield:** Adrenergic receptor distribution and effects: | Receptor | Location | Effect | Mechanism | |----------|----------|--------|----------| | **α1** | Vascular smooth muscle, pupil dilator | Vasoconstriction, mydriasis | ↑ IP3/DAG → ↑ [Ca²⁺]i | | **α2** | Presynaptic terminals, platelets | Inhibition of NE release, platelet aggregation | ↓ cAMP (Gi coupling) | | **β1** | Heart, kidney | ↑ HR, ↑ contractility, ↑ renin | ↑ cAMP (Gs coupling) | | **β2** | Bronchi, blood vessels | Bronchodilation, vasodilation | ↑ cAMP (Gs coupling) | **Mnemonic:** **ABCD of α1 effects** — Arteries (vasoconstriction), Blood pressure (↑), Contraction of smooth muscle, Dilation of pupil (mydriasis) **Clinical Pearl:** Selective α1-blockers (prazosin, doxazosin) cause vasodilation and are used in hypertension and benign prostatic hyperplasia. Non-selective α-blockers (phentolamine) are used acutely in pheochromocytoma crisis.
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