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61 Cards in this Set

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Epinephrine
*Heart (β1): ↑automaticity, ↑HR, ↑conduction velocity, ↑CO (β1 stimulated ↑ in contractility + relaxation in blood vessels due to β2 stimulation @ therapeutic dose), ↑O2 consumption, ↓efficiency
*BP (β2 & α1): ↓ @ low [ ] via β2 dilation, ↑ as [ ] ↑ & α1 receptors become occupied; If both receptors occupied – α1 response predominates; @ low [ ] MBP is often ↓, @ high [ ] MBP is ↑
*Respiratory tract (β2 & α1): bronchioles dilated via β2 – most prominent when bronchial muscle is constricted due to drugs/disease; secretions ↓ via α1
Metabolism: ↑ glycogen breakdown (β2); ↓ glycogen synthesis (α1); ↓ insulin secretion (α2), ↑ free fatty acids (β3)
Norepinephrine
*Heart(β1): direct effects; same as epi
*BP (α1): ↑ systolic, diastolic and mean
*Cardiac Output: no change or slightly ↓ due to α1 mediated constriction of blood vessels
*Metabolism; ↓ glycogen synthase activity via α1
Isoproterenol
*Heart (β1) – direct effects same as epi
BP (β2): ↓BP
Respiratory Tract (β2): relaxes bronchi
Dopamine
*Receptors activated (DA, β1, β2, α1 @ ↑ [ ])
Heart (β1): HR ↑
BP: ↓ by DA receptor activation in renal/mesenteric beds; ↓ by β2 receptor activation; ↑ by ↑↑↑ [ ] by α1 receptor activation
Dobutamine
*Heart (β1*) – greater inotropic (contractility) than chronotropic (rate) effects; ↑↑ [ ] may also ↑ automaticity
*BP: ↑ [ ] can ↑ BP via α1
Phenylephrine
*Non-catecholamine α stimulators are NOT metabolized by COMT
Ephedrine
Clonidine
*Brain: α2 @ receptors sites block sympathetic output – postsynaptic
α-Methyldopa
*Periphery: α2 act @ presynaptic receptors to inhibit NE release
Terbutaline
Albuterol
Amphetamine
*Displaces NE from terminal à sympathomimetic effects
*Substrate for NET and ↑ synaptic NE via facilitated exchange diffusion
Methylphenidate
Prazosin
*Block α1 receptors only
*α1 blockade: ↓BP, get reflex tachycardia
Phenoxybezamine
*Block α1 receptors only
*Duration of action ~24 hrs
*Must synthesize new receptor to recover α1 effect
Phentolamine
*Block α1 and α2 receptors
*α1 blockade ↓ BP
*α2 blockade prevents feedback inhibition by released NE, causing more NE to be released onto β receptors in heart, producing even GREATER TACHYCARDIA than w/ a selective blocker
Propanolol
*Blocks β1 and β2
*Cardiac effects: ↓ HR due to β1 block; ↓ CO (more pronounced during exercise); ↓ conduction velocity, myocardial O2 demand, & spontaneous rate of depolarization
*Vascular & BP Effects: β2 may ↑ TPR slightly; ↓ plasma rennin due to β1 block; net effect BP ↓
*Metabolic Effects: no effect on plasma glucose in normal, but does slow recovery from hypoglycemia in diabetics (less of a problem w/ β selectives); ↑ plasma [ ] of triglycerides (VLDL) and ↓ [ ] HDL
*Respiratory Tract (β2 block): airway resistance ↑; can be life threatening in asthmatics
Atenolol
*Cardiac effects: similar to non-selective β blockers
Esmolol
*Less danger of respiratory side effects than w/ non-selective
Timolol
*At ↑ [ ] à NO β blocker is really “selective”
(nonselective)
Caffeine
*CNS: all cortical areas are sensitize; ↑ [ ] sensitize the respiratory areas to CO2 & ↑ respiratory rate
*CV: ↑ HR and ↑ contractility; systemic BV dilate; TPR ↓ (looks like β2 stimulation); cerebral blood vessels constricted; net effect à BP ↑ because caffeine releases catecholamines
Theophylline
*Respiratory tract: bronchi relaxed
Guanethidine
Enters via NET, uncouples AP from Ca++ entry, and stabilizes vesicular membrane; stops NE from being stored; ↓BP
Reserpine
Enters the terminal (lipid soluble), stabilizes vesicular membrane, causing depletion of NE over time; stops NE from being stored
Tyramine
Cause displacement of NE from terminal à sypathomimetic effects
*normally metabolized by monamine oxidase in the gut
*In CNS metabolized to octopamine which is stored in vesicles causing displacement of NE
Cocaine
*Blocks NET à ↑ synaptic NE
Imipramine
*Blocks NET à ↑ synaptic NE
Atomoxetine
*Blocks NET à ↑ synaptic NE
(selective NE reuptake inhibitor)