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    Subjects/Pharmacology/Receptor Subtypes and Pharmacological Effects
    Receptor Subtypes and Pharmacological Effects
    medium
    pill Pharmacology

    Regarding alpha-adrenergic receptor subtypes and their pharmacological effects, all of the following statements are correct EXCEPT:

    A. Alpha-2 receptors are located presynaptically on noradrenergic neurons and inhibit norepinephrine release
    B. Alpha-1 antagonists like prazosin cause reflex tachycardia due to loss of negative feedback on sympathetic outflow
    C. Alpha-1 receptors mediate vasoconstriction and are coupled to phospholipase C via Gq proteins
    D. Alpha-2 agonists such as clonidine cause mydriasis and are used as first-line agents for hypertension

    Explanation

    ## Alpha-Adrenergic Receptor Subtypes: Classification and Effects ### Alpha-1 Receptors **Key Point:** Alpha-1 receptors are postsynaptic, coupled to Gq/phospholipase C, and mediate vasoconstriction, mydriasis, and increased cardiac contractility. - **Location:** Postsynaptic vascular smooth muscle, iris dilator muscle, heart - **G-protein coupling:** Gq → ↑ IP₃/DAG → ↑ intracellular Ca²⁺ - **Effects:** Vasoconstriction, mydriasis, positive inotropism - **Antagonists:** Prazosin, doxazosin, terazosin - **Side effect of antagonists:** Reflex tachycardia (due to vasodilation → ↓ BP → baroreceptor activation) ### Alpha-2 Receptors **Key Point:** Alpha-2 receptors are presynaptic inhibitory autoreceptors coupled to Gi/Go, which decrease cAMP and inhibit neurotransmitter release. - **Location:** Presynaptic nerve terminals (noradrenergic, serotonergic, cholinergic neurons), postsynaptic CNS - **G-protein coupling:** Gi/Go → ↓ cAMP → hyperpolarization - **Presynaptic effect:** Negative feedback inhibition of norepinephrine release - **Central effects:** Sedation, analgesia, anxiolysis - **Agonists:** Clonidine, dexmedetomidine, methyldopa ### Why the Correct Answer is Wrong **High-Yield:** Alpha-2 agonists cause **miosis** (pupillary constriction), NOT mydriasis. This is a classic exam trap. - Clonidine activates presynaptic alpha-2 receptors in the locus coeruleus → ↓ sympathetic outflow → ↓ norepinephrine at the iris dilator muscle → **miosis** - Mydriasis (pupil dilation) is caused by **alpha-1 agonists** (e.g., phenylephrine) or **loss of parasympathetic tone** (anticholinergics) - Clonidine is NOT a first-line agent for hypertension; it is reserved for resistant hypertension or specific indications (e.g., ADHD, opioid withdrawal) due to risk of rebound hypertension on abrupt withdrawal ### Comparison Table: Alpha Receptor Effects | Feature | Alpha-1 | Alpha-2 | | --- | --- | --- | | **Location** | Postsynaptic (vascular, cardiac) | Presynaptic (autoreceptor) | | **G-protein** | Gq | Gi/Go | | **Second messenger** | ↑ IP₃/DAG | ↓ cAMP | | **Vascular effect** | Vasoconstriction | Vasodilation (CNS) / presynaptic inhibition | | **Pupil effect** | Mydriasis | Miosis | | **Agonist example** | Phenylephrine | Clonidine | | **Antagonist example** | Prazosin | Yohimbine | **Clinical Pearl:** Clonidine withdrawal causes severe rebound hypertension due to unopposed alpha-1 effects—always taper gradually and counsel patients on adherence.

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