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  1. Reserpine blocks the granular (vesicular) uptake of nor-epinephrine by blocking VMAT (vesicular monoamine transporter), thus exposing the monoamines to cytoplasmic degradation and depleting their overall availability for adrenergic activity.
  2. The principal process which terminates the action of noradrenaline released from adrenergic nerve ending is axonal uptake.
  3. The rate limiting enzyme in the synthesis of catecholamines is tyrosine hydroxylase.
  4. The most efficacious inhibitor of catecholamine synthesis in the body is α-methyl-p-tyrosine.
  5. The α-2 adrenoceptors are prejunctional (adrenergic nerve endings), postjunctional (brain, pancreatic B cells) as well as extrajunctional (certain blood vessels, platelets) in location.
  6. Noradrenaline is administered by slow intravenous infusion.
  7. Blood vessels have a-1 and b-2 receptors on them. The former are stronger (needs high dose of agonist) and upon activation causes vasoconstriction while the latter are sensitive (even in small doses of agonist) and upon activation causes vasodilation.
  8. Ephedrine is similar to adrenaline in producing both α and β adrenergic effects.
  9. Phenylephrine instilled in the eye produces mydriasis but no cycloplegia.
  10. Mephentermine is a pressor agent that acts directly as well as indirectly and produces both vasoconstriction and cardiac stimulation and can be given by IM injection to a patient undergoing a surgical procedure that develops hypotension to raise his BP.