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Yr 1 - Membranes, Lipids, Signalling > Extracellular Signalling - Receptors > Flashcards

Extracellular Signalling - Receptors Flashcards

1
Q

How is the specificity of hormonal action achieved?

A

Through interaction with its complementary receptor

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2
Q

How can different cells respond differently to the same hormone?

A

There are multiple receptor subtypes within their own transduction mechanisms

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3
Q

What is effect of adrenaline in:

  1. Muscle and liver
  2. Adipose tissue
  3. Cardiomyoctyes
A
  1. Stimulates breakdown of glycogen
  2. Stimulates fatty acid production in adipose tissue
  3. Increased heart rate and blood pressure by stimulating vascular smooth muscle cells
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4
Q

What are the 4 main classes of receptors?

A
  1. Ligand-gated ion channel (ionotropic receptors)
  2. G-protein coupled receptor
  3. Receptor tyrosine kinase
  4. Nuclear hormone receptor
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5
Q

What receptors are cell surface receptors?

A
  1. Ligand-gated ion channel
  2. G protein-coupled receptor
  3. Receptor tyrosine kinase
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6
Q

What receptors are intracellular receptors?

A

Nuclear hormone receptor

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7
Q

What signalling molecules are cell surface receptors for?

A

Hydrophilic signalling molecules

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8
Q

What are signalling molecules are intracellular receptors for?

A

Lipid-based (lipophilic/hydrophobic) signalling molecules

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9
Q

Describe opening of ligand-gated ion channels

A

Open and close in response to shift in membrane potential

  1. Binding causes conformational change in the channel protein allowing the opening of ion channels
  2. Specific ions (Na+, K+, Ca2+) flow through channel (in or out)
  3. Alters cells electric potential (membrane potential)
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10
Q

What do ligand-gated ion channels allow?

A

Rapid synaptic signalling between electrically excitable cells

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11
Q

What type of receptor is nAChR?

A

Ligand-gated ion channel (ionotropic receptor)

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12
Q

How is nAChR activated?

A

There are 2 binding sites and both must be occupied for the receptor to become activated

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13
Q

How does nAChR cause membrane depolarisation?

A

Increased Na+ and K+ permeability –> Na+ moves in and K+ moves out of cell

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14
Q

What is the Renin-Angiotensin System stimulated by?

A

Decrease in blood pressure / blood Na+ or blood volume

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15
Q

What are the 2 main enzymes involved in the RAS?

A

Renin and angiotensin-converting enzyme (ACE)

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16
Q

How does decrease in blood pressure affect RAS?

A
  1. Decrease in blood pressure detected by kidneys
  2. Causes release of renin cleaves angiotensin I from N-terminus of angiotensinogen via the liver
  3. ACE cleaves angiotensin II from angiotensin I
  4. Angiotensin II causes secretion of aldosterone from adrenal cortex
  5. Aldosterone has role in water reabsorption and decreases during volume –> increases blood pressure
17
Q

What type of receptors are Ang II?

A

GPCRs –> AT1 and AT2

18
Q

What effects are mediated by AT1 receptor activation?

A
  1. Vasoconstriction
  2. Increased noradrenaline release from sympathetic nerve terminals
  3. Aldosterone secretion from adrenal cortex
  4. Vascular growth
19
Q

What effects are mediated by AT2 receptor activation?

A

Anti-hypertrophic and anti-hypertensive effects (AT2 receptor activation opposes the effects of AT1 receptor activation)

20
Q

Does AT1 or AT2 have a higher affinity for Ang II?

A

Similar affinity but only share 30% sequence identity

21
Q

What are catalytic receptors?

A

Receptor itself is an enzyme

22
Q

What are examples of catalytic receptors?

A
  1. Tyrosine kinase receptors
  2. Serine/Threonine kinase receptors
  3. cGMP-linked receptors
23
Q

How do non-catalytic receptors act?

A

Through cytoplasmic tyrosine kinases

24
Q

What are examples of non-catalytic receptors?

A
  1. Cytokines
  2. Growth hormone
  3. Prolactin
25
Q

What are tyrosine kinase receptors activated by?

A

Insulin and growth factors

26
Q

What is effect of kinase-linked receptors?

A

Act by indirectly regulating gene transcription

27
Q

What is function of nuclear hormone receptors?

A

Regulate gene transcription

28
Q

What is structure of nuclear hormone receptors?

A

Monomeric structure - separate ligand and DNA-binding domains

29
Q

How do hormones interact with nuclear hormone receptors?

A
  1. Hormones diffuse across plasma membrane and interact with intracellular receptors
  2. Form hormone-receptor complexes
  3. Bind to regions of DNA (‘hormone responsive elements’) and affect gene transcription
30
Q

What are the 2 classes of intracellular receptors?

A
  1. Cytosolic (steroid)

2. Nuclear (thyroid)

31
Q

What are the targets of G protein-coupled receptors (GPCRs)?

A

Peptide hormones, neurotransmitters

32
Q

How do G-protein receptors work?

A
  1. Binding of ligand results in conformational change of receptor
  2. Facilitates interaction with signal-transducing heterotrimeric G-protein
  3. In turn, modulates the activation or inhibition of downstream effector proteins
  4. These effector proteins modulate the levels of 2nd messenger molecules
33
Q

What are 2nd messengers?

A

A small intracellular molecule formed transiently in response to receptor activation e.g. cAMP, cGMP, IP3, DAG and Ca2+

34
Q

How do AT1 receptor antagonists work?

A

Bind selectively to AT1- receptors and thus inhibit the effects of angiotensin II

35
Q

How do aldosterone receptor antagonists work?

A

Blocks the action of aldosterone at mineralocorticoid receptors. This group of drugs is often used as adjunctive therapy for the management of chronic heart failure

36
Q

How do ACE inhibitors work?

A

Prevent production of angiotensin II

As a result, blood vessels enlarge or dilate, and blood pressure is reduced. This lower blood pressure makes it easier for the heart to pump blood and can improve the function of a failing heart.

Used to treat high blood pressure and heart failure

Yr 1 - Membranes, Lipids, Signalling (24 decks)

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