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18 Cards in this Set

  • Front
  • Back
Mechanism of Action for Albuterol (al byoo’ ter ole)
Albuterol, as well as terbutaline, selectively activates beta2-receptors, and thus causes fewer cardiac effects than less selective adrenergic agonists.
Mechanism of Action for Amphetamine (am fet’ a meen)
Amphetamine induces the release of catecholamines from adrenergic synapses.
Mechanism of Action for Atenolol (a ten’ oh lole)
Atenolol is a selective beta1-receptor antagonist have an intermediate half-life (4 to 9 hrs).
Mechanism of Action for Atropine (a’ troe peen)
Selectively antagonizes muscarinic receptors (limited to the peripheral effects at clinical doses)
Mechanism of Action for Baclofen (bak’ loe fen)
Baclofen activates presynaptic GABA-B receptors that restrict calcium influx, thereby decreasing release of excitatory neurotransmitters, and it activates postsynaptic GABA-B receptors that increase potassium conductance, thereby hyperpolarizing the membrane, thus further enhancing the inhibitory effect.
Mechanism of Action for Bromocriptine (broe moe krip’ teen)
Bromocriptine is a potent agonist of D2 receptors, which are said to open potassium channels via the Gi coupling protein.
Mechanism of Action for Capsaicin (kap say’ uh sin)
Capsaicin causes the release of peptide substance P from sensory neurons.
Mechanism of Action for Clonidine (kloe’ ni deen)
Clonidine activates presynaptic alpha2-receptors in the vasomotor center of the brainstem. These receptors restrict calcium influx, thereby decreasing the release of norepinephrine, thus reducing sympathetic outflow from the CNS, resulting in the antihypertensive effects of decreased cardiac output and reduced peripheral vascular resistance.
Mechanism of Action for Cocaine (koe kane’)
Cocaine inhibits dopamine transporter (DAT), norepinephrine transporter (NET), and serotonin transporter (SERT) allowing these catecholamines to remain in the synaptic cleft longer, thus potentiating neurotransmission at adrenergic synapses.
Mechanism of Action for Naloxone (nal’ ox ohn)
Naloxone antagonizes opioid effects by competing for mu, kappa, and sigma opiate receptor sites in the CNS, having the greatest affinity for the mu receptors.
Mechanism of Action for Nicotine (nik’ oh teen)
Agonist at both NN and NM receptors
Mechanism of Action for Ondansetron (on dan’ se tron)
Ondansetron is a competitive, highly selective antagonist of the uniquely ionotropic, 5-HT3 receptors. Stimulation of 5-HT3 receptors activates the vomiting center of the brain, thus blocking these receptors results in an antiemetic effect.
Mechanism of Action for Phenylephrine (fen il ef’ rin)
Phenylephrine, like oxymetazoline & tetrahydrazoline, is a selective alpha1-receptor agonist.
Mechanism of Action for Prazosin (pra’ zoe sin)
Prazosin, like terazosin & doxazosin, is a selective antagonist of alpha1-receptors in arterioles and veins (1000-fold greater affinity for alpha1 than alpha2).
Mechanism of Action for Ranitidine (ra nye’ te deen)
Ranitidine is an H2 receptor antagonist.
Mechanism of Action for Reserpine (re ser’ peen)
Reserpine irreversibly damages vesicular monoamine transporters (VMAT-1 & VMAT-2) that concentrate NE, serotonin, & dopamine in vesicles, thus leading to their depletion in adrenergic terminals via intraneuronal, mitochondrial MAO metabolism.
Mechanism of Action for Strychnine (strik’ neen)
Strychnine selectively blocks the pentameric receptors of the inhibitory transmitter glycine that hyperpolarizes spinal interneurons – as well as some of the brainstem – via increasing chloride conductance. The removal of that hyperpolarizing effect leads to convulsive action.
Mechanism of Action for Yohimbine (yo him’ bean)
Yohimbine blockades alpha2-autoreceptors in the vasomotor center of the brainstem, preventing them from restricting calcium influx, leading to increased release of NE, enhancing sympathetic outflow from the CNS, stimulating cardiac beta1-receptors and peripheral vasculature alpha1-receptors, causing a rise in blood pressure. Yohimbine also causes increased insulin release through blockade of suppressive alpha2-receptors in the pancreatic islets.