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aa PA30251 > Receptor theory 1 > Flashcards

Receptor theory 1 Flashcards

1
Q

Give 5 examples of Pre 19th century plant extracts used to begin to explore the effects of natural substances

A
  1. Quinine (alkaloid from cinchona bark)
  2. Digitalis (Purple foxglove Digitalis purpurea)
  3. Atropine (Deadly nightshade Atropa belladonna)
  4. Ephedrine (active principle of the herb ‘ma-huang’, Ephedra)
  5. Strychnine (alkaloid from the seeds of Nux vomica)
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2
Q

What did Humphrey Davy do

A
  1. Prepared nitrous oxide (laughing gas) to liven up parties (1799). Introduced as an anaesthetic in 19th century
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3
Q

What did Friedrich Serturner do

A
  1. Purified morphine from opium (1805).
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4
Q

What did Claude Bernard do

A
  1. Skeletal muscle treated with curare failed to respond to electrical stimulation of its nerve (1851).
  2. Curare had no action on nerve alone.
  3. Site of paralysis at junction between nerve and muscle.
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5
Q

What are the two theories about how nerve impulse transmitted across gap

A
  1. Electrical
  2. Humoral
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6
Q

What did Matteucci (1811-1868) discover

A
  1. The nerve of a nerve-muscle preparation is laid across a beating heart.
  2. Electrical action currents spreading through the heart stimulate the nerve and so induce contractions in the muscle in time with the heart beats.
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7
Q

What is the Electrical theory of neurotransmission

A
  1. Electrical current from a large muscle mass may excite a nerve.
  2. Effect should be bi-directional.
  3. However, the current in the nerve is too small to excite a muscle; amplification required.
  4. Amplification occurs at the nerve/muscle junction and is achieved chemically.
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8
Q

What is the Humoral (chemical) theory of neurotransmission

A
  1. Transmission across the gap is uni-directional.
  2. Delay in transmission across the gap.
  3. Fatigue occurs more readily at junctions.
  4. Drugs may act selectively at synapses/junctions.
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9
Q

What did Oswalt Schmiedeberg (1838-1920)

A
  1. The alkaloid, muscarine, extracted from the toadstool, Amanita muscaria, resembled to effects of vagal stimulation. (decreases heart rate)
  2. Suggested that muscarine stimulated the vagus nerve endings.
  3. It was later shown that a muscarine-like substance was released from frog heart when the vagus nerve was stimulated (Dixon, 1908).
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10
Q

What new synthetic drugs appeared in 20th century from synthetic chem

A
  1. Barbiturates
  2. Local anaesthetics
  3. Antimicrobial chemotherapy
  4. Antibacterial
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11
Q

What did Paul Ehrlich (1845-1915) do

A
  1. Studies with dyes and bacteria formed the bases of ideas on the recognition of biological substances by chemicals.- bind to cell walls
  2. ‘Corpora non agunt nisi fixata’ - (A drug will not work unless it is bound) – idea of specific recognition sites for drugs in order to act
  3. He proposed a collection of “amboceptors, triceptors and poloyceptors” on cells for dyes = chemoreceptors.
  4. Discovered arsenical compounds for the treatment of syphilis (1909).
  5. 1908, awarded Nobel prize for medicine.
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12
Q

What did Sir Henry Dale (1875-1968) do

A
  1. Studies on histamine (1911) and acetylcholine (1914).
  2. ACh equipotent with muscarine.
  3. ACh mimicked parasympathetic nerve stimulation (muscarinic or parasympathomimetic).
  4. Low doses of ACh blocked by atropine.
  5. High doses then mimicked effects of nicotine (stimulation of sympathetic ganglionic cells).
  6. ACh and nicotine also stimulated skeletal muscle and parasymapthetic ganglia. These actions of ACh are termed nicotinic
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13
Q

What did Otto Loewi (1876-1961) do

A
  1. First evidence of chemical transmission (1921)
  2. Loewi’s perfused frog heart experiments 1 &2
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14
Q

Describe Loewi’s perfused frog heart experiments

A
  1. Vagal stimulation slows heart 1, shortly after heart 2 slows also.
  2. Concluded that a substance (Vagusstoff) was released from nerve endings of heart 1 and conveyed to heart 2 in perfusion fluid.
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15
Q

Describe Loewi’s perfused frog heart experiments 2

A
  1. Stimulation of accelerans nerve (sympathetic) increases rate of heart 1, shortly after heart 2 beat more rapidly.
  2. Concluded that another substance (Acceleranstoff) was released from sympathetic nerve endings; similar to adrenaline.
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16
Q

What were Dale and Loewi’s findings

A
  1. Loewi showed that Vagusstoff and ACh had similar actions.
  2. Effects of both were blocked by atropine and potentiated by physostigmine (inhibits cholinesterase which hydrolyses ACh).
  3. Acceleranstoff argued to be similar to adrenaline.
  4. Dale classified nerve fibres which release ACh as cholinergic, those which release an adrenaline-like substance as adrenergic.
  5. Chemical communication therefore has a central role in almost every regulatory mechanism in our body.
17
Q

What did John Newport Langley (1852-1926) do in terms of receptor theory

A
    1. Applied nicotine to frog skeletal muscle. The muscle only contracted when nicotine was applied in the region of the motor end-plate.
  2. Hypothesised that ACh was combining with a “receptive substance” in this region.
  3. Introduced the concept of receptors for chemical mediators.
  4. Suggested that receptors were switches that received and generated signals, and which could be activated or blocked by specific molecules
18
Q

What did Alfred J Clark (1885-1941) do

A
  1. Originator of quantitative receptor theory developed by applying chemical laws to biological phenomena.
  2. Suggested that measurable drug-evoked responses in tissues resulted from the unimolecular interaction of the drug and a substance on the cell surface.
19
Q

Describe drug interactions with organ systems

A
  1. Drugs modify the function of different organ systems- CVS, GIT, CNS etc.
  2. Change in organ function is achieved by pharmacodynamic interaction between the drug and the biological recognition system for that drug.
  3. Even though drugs exhibit organ specificity, the underlying principles of the pharmacodynamic interaction are the same.
  4. Organ selectivity determined by the biological recognition unit for the drug = receptor.
20
Q

What is a receptor

A
  1. A macromolecule with which a drug combines to produce it’s characteristic effects.
21
Q

What are the 4 kinds of regulatory protein (drug targets)

A
  1. Enzymes
  2. Carrier molecules
  3. Ion channels
  4. Receptors
22
Q

What are the rules for regulatory proteins

A
  1. Specificity is reciprocal
  2. No drug is completely specific
23
Q

What does affinity mean

A
  1. If a molecule closely associates with a receptor protein it has affinity for that receptor.
24
Q

What is an antagonist

A
  1. If no stimulus is elicited than no response- antagonists (drugs which produce no response and block responses induced by agonists).
  2. Have affinity for receptor but no intrinsic efficacy.
25
Q

How can the result of the drug-receptor interaction be measured?

A
  1. Kymograph- used to be used to measure smooth muscle contraction
  2. Isotonic transducer- measuring tissue which contracts and changes its length
  3. Isometric transducer- measuring tissue which changes tension
  4. Blood pressure transducer
26
Q

What is EC50

A
  1. EC50= Concentration of drug required to induce 50% maximal response- found by drawing arrow from 50 to curve and down to drug concentration
  2. Can be used to compare drug potency- concentration required to have effect
27
Q

What is drug potency

A
  1. Potency is a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity.
  2. Drug potency can be described as pEC50 (Negative log of Drug concentration to elicit 50% maximal response
27
Q

What is drug potency

A
  1. Potency is a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity.
  2. Drug potency can be described as pEC50 (Negative log of Drug concentration to elicit 50% maximal response
28
Q

What is intrinsic efficacy

A
  1. Intrinsic efficacy- stimulant ability of agonists
  2. Describes the tendency of a drug-receptor complex to form the active AR* state rather than resting AR state
  3. A drug with 0 efficacy has no tendency to cause receptor activation
  4. A full agonist is a drug whose efficacy is sufficient to cause maximum response when less than 100% of receptors are occupied
  5. A partial agonist has lower efficacy such that 100% occupancy elicits only a sub-maximal response
29
Q

Describe the different agonist drug potency:
1. Drug A: EC50 = 2.70 nM (2.710-9M)
2. Drug B: EC50 = 95.0 nM (9.510-8M)

A
  1. Drug A is approx 35 times more potent than Drug B
30
Q

Give the pEC50 values for these 2 drugs
1. Drug A: EC50 = 2.70 nM (2.710-9M)
2. Drug B: EC50 = 95.0 nM (9.510-8M)

A
  1. pD2 values or pEC50 = negative Log10 of [Drug] to elicit 50% maximal response
  2. Drug A: pEC50 = 8.56
  3. Drug B: pEC50 = 7.02
  4. Take negative log from M concentration
31
Q

What is an antagonist

A
  1. Drugs which bind to the receptor but elicit no response themselves block responses induced by agonists, and are known as antagonists.
  2. Receptor antagonists will have affinity for the receptor but no intrinsic efficacy.
32
Q

What happens to a response concentration durg curve in presence of an antagonist

A
  1. Dose response curves for Drug A (+/- Drug B) are parallel- shifts to the right
  2. Drug A and Drug B compete for the same binding site on the receptor.
  3. Drug B is a competative antagonist of Drug A
33
Q

Describe partial Agonist-receptor interactions

A
  1. These ligands,exhibit some agonist activity but fail to elicit full responses, and block responses induced by full agonists at the receptor.
  2. These compounds are known as partial agonists.
    activity
    3, In vivo, the balance between agonist and antagonist activity will depend on the level of transmitter activity at the receptor and the relative levels of affinity and efficacy of the partial agonist.
34
Q

Define strong partial and weak partial agonists

A
  1. Strong partial agonists: - strong agonist, weak antagonist activity
  2. Weak partial agonists:- weak agonist, strong antagonist
35
Q

What did James Black do

A
  1. You can take an agonist that produces a response you want to block
  2. Modify its structure
  3. Maintaining or improving affinity
  4. But losing the intrinsic energy- losing efficacy
  5. Changing it from agonist to antagonist
  6. He did with histamine -> cimetidine

aa PA30251 (9 decks)

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