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Drilldown: Medicines

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Medicines > pregnancy : Category B or Category C

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Agonist at the metabotropic GABAB receptor and the endogenous γ-hydroxybutyrate (GHB) receptor. Produces deep sleep with increased slow-wave architecture, suppression of REM intrusion, and cataplexy reduction. (1) · Cardioselective β1-adrenergic antagonist. Selectivity is dose-dependent and partially lost at higher doses. (1) · High-affinity D2 receptor antagonist (1) · Highly β1-selective adrenergic antagonist. Greater selectivity than metoprolol or atenolol. (1) · Non-selective competitive antagonist at β1 and β2 adrenergic receptors. Lipophilic; significant blood–brain barrier penetration, accounting for its CNS effects. (1) · Norepinephrine–dopamine reuptake inhibition (DAT, NET), d-threo enantiomer of methylphenidate (1) · Selective alpha-1 adrenergic receptor antagonist. Lowers peripheral vascular resistance via vasodilation; in the CNS, blunts noradrenergic hyperarousal thought to drive trauma-related nightmares. (1) · Selective inhibitor of PDE5 with a substantially longer half-life than other PDE5 inhibitors, allowing once-daily continuous dosing. (1) · Selective inhibitor of PDE5. Slightly higher PDE5/PDE6 selectivity vs sildenafil (less visual side effect) but more PDE1 cross-activity (occasional QT effects at high doses). (1) · Selective inhibitor of phosphodiesterase type 5 (PDE5), preventing cGMP breakdown in vascular smooth muscle. In the corpus cavernosum, potentiates the NO/cGMP cascade triggered by sexual stimulation. (1) · Serotonin–norepinephrine reuptake inhibition (balanced) (1) · TAAR1 agonism, VMAT2 substrate, DAT/NET reverse transport, net release of dopamine and norepinephrine (1) · The d-enantiomer is a highly β1-selective antagonist; the l-enantiomer triggers endothelial nitric-oxide–mediated vasodilation. Unique among beta blockers for this NO mechanism. (1)
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