Week 3 Flashcards
Alpha 1 receptors
Adrenergic receptors
Norepinephrine and Epi binds to these receptors.
Activation leads to sympathetic response.
Fight or flight– need increased BP, to see more, don’t pee yourself, more more glucose
Vasoconstriction
Pupil dilation
Urinary retention and contraction
Glycogenolysis in liver- glucose production
Inhibition of renin release in kidney (regulation of BP)
Alpha 2 receptors
Adrenergic receptor
GI protein-coupled receptors
Located on presynaptic nerve endings, and when activated cause decrease in intracellular CAMP, which inhibits further release of norepi.
Also located on pancreatic outlets and lead to decreased insulin secretion.
Beta 1 receptors
Adrenergic receptor
Located on heart and when activated, lead to increase HR, contractility, and AV node conduction.
Also on kidneys, which lead to increased renin, which increases BP.
Beta 2 receptors
Adrenergic receptors Lung- bronchodilation Skeletal muscle-relaxation-vasodilation Smooth muscle in GI and uterus- decreased GI motility and inhibition of labor. Pancreas- increase in insulin secretion
Adrenergic agonists
Catecholamine and noncatecholamine. Differ in oral usability, duration of action, and CNS penetration.
3 types:
Direct acting agonists
Indirect acting agonists
Mixed-action agonists
Cells become desensitized if exposed for too long.
Direct acting adrenergic agonists NON-SELECTIVE
Non-selective (can act of alpha or beta)
Catecholamines (only by injection)
Binds to alpha or beta receptor and mimic effects of epinephrine, norepinephrine, and dopamine in our bodies.
Most common:
epinephrine
Acts on beta and alpha. Leads to vasoconstriction, increased cardiac output, bronchodilation (alpha)
Norepinephrine: mostly stimulates beta. Vasoconstriction and increase in BP
Dopamine: stimulates all 3 in dose-dependent manner. Low dose stimulates dopa receptors, higher doses stimulates B1, then A1
Indirect acting adrenergic agonists
Enhance effects of epi and norepinephrine by inhibiting their reuptake or degradation (by MAOs). Don’t work directly on postsynaptic receptors.
Cocaine and amphetamines
Stimulate alpha 1 and beta 1 which stimulates a sympathetic response. Increase in BP and HR
Mixed-action adrenergic agonists
Stimulation of adrenergic receptors by Direct binding and as well as release of stored norepinephrine from presynaptic terminals.
Ephedrine and pseudoephedrine. Noncatecholamines long-acting.
Alpha1 antagonists (blockers)
(-osin)
Adrenergic antagonist
Can be selective or non-selective
Reversible block effects of catecholamines at the post-synaptic alpha1 receptors in vascular smooth muscle and bladder neck and prostate.
(-osin) vascular smooth muscle. Decrease BP and vascular resistance. Relief of urinary difficulty in BPH. prazosin, doxazosin (good tx for HTN) tamsulosin (good for BPH), etc. can block receptors in different sites which is why some are better for HTN and some are better for BPH. Side effects or this tactic hypotension.
Alpha2 blockers- not used in humans
Doxazosin
Alpha1 selective antagonist (alpha1 blocker). Relaxes vascular smooth muscle, leading to decrease peripheral resistance and decreased BP.
Side effects: orthostatic hypotension, HA, and nasal congestion.
Beta blockers
Selective and non-selective. Also grouped into generations.
Competitive inhibitors of beta adrenergic receptors. Prevent catecholemines like epi and norepinephrine, as well as other beta agonists from binding.
Decrease HR, contractility of ventricles, AV conduction, decreases peripheral resistance, decreases BP (through decreases renin), increased bronchial constriction, decreased intraoccular pressure, and inhibition of lipolysis.
HTN, CHF, etc. also used in glaucoma and migraine prophylaxis.
Propranolol is the prototype
Onset of action: 1-2 hrs orally. Rapidly absorbed.
Half-life 3-6 hrs
Excreted in urine
Drug interactions: alcohol, nitrates, cold remedies, Clonidine
Don’t take within 8 hrs of another dose. Food enhances bioavailability
1st generation beta blockers (nonselective)
Block b1 and b2.
Propanolol, sotalol, basilisk, timolol.
Can also penetrate CNS which is why it is effective in migraine prophylaxis.
Mostly effective on B1, leading to decreased HR, contractility, and BP. however the effects on B2 cause bronchoconstriction, so not recommended for people with COPD or asthma
Beta1- dobutamine. Increased HR and COP, acute CHF.
2nd generation (beta-1 selective)
Cardioselective BB
more suitable for people with chronic respiratory conditions. However with increased doses, B1 selectivity can be lost.
Atenolol, esmolol, metoprolol, acebutolol, bispropolol.
3rd generation beta blockers
Both non selective and selective BB. also act on blood vessels to create vasodilation (alpha). Very effective in treating HTN. especially in CHF patients.
Non-selective: Carvedilol and labetolol. Peripheral vasodilation by blocking beta and alpha 1
B1 selective- nebivolol and betaxolol. Produce vasodilation.
Sympathetic (adrenergic) nervous system
Part of the autonomic nervous system. Sympathetic neurons come from thoracic and lumbar regions of the spinal cord.
Epinephrine and norepinephrine activate alpha, beta, and dopamine receptors, called adrenergic receptors
Fight or flight. Dilation of pupils, inhibition of saliva, relaxation of the airways, acceleration of the heart, inhibition of digestion, stimulation of glucose release in the liver, inhibition of intestinal activity, inhibition of gallbladder, stimulation of adrenal medulla (secretion of epi and norepinephrine), relaxation of bladder, and stimulation of ejaculation or vaginal contractions.
Parasympathetic (cholinergic) nervous system
Part of autonomic nervous system.
Releases ACh- counterbalances sympathetic activity.
Activates muscarinic receptors and nicotinic receptors (cholinergic receptors).
Rest and digest. Feed and breed.
