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Pharm > Lecture 10: Drugs to Treat High BP II > Flashcards

Lecture 10: Drugs to Treat High BP II Flashcards

1
Q

What are the three types of adrenergic receptors?

A
  • Alpha 1
  • Beta 1
  • Beta 2
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2
Q

What are the effects when an agonist binds to alpha 1 receptors?

A

Vasoconstriction of organs that are no required for the fight of flight response

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3
Q

What are the effects when an antagonist binds to alpha 1 receptors?

A

Vasodilation of organs that are not required for the fight or flight response

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4
Q

What are the effects when an antagonist bind to beta 1 receptors?

A

Increased cardiac contractility and rate

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5
Q

What are the effects when an antagonist binds to beta 1 receptors?

A

Decreases cardiac contractility and rate

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6
Q

What are the effects when an agonist binds to beta 2 receptors?

A

Relaxation of airway vascular smooth muscle

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7
Q

What are the effects when an antagonist binds to beta 2 receptors?

A

Constriction of the airway vascular smooth muscle

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8
Q

Where are beta 1 receptors found?

A

In the heart

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9
Q

Where are Beta 2 receptors found?

A

In the lungs

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10
Q

What is the main effect of beta blockers?

A

Decrease cardiac output by decreasing contractility and heart rate

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11
Q

What does RAAS stand for?

A

Renin Angiotensin Aldosterone System

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12
Q

What does the RAAS system control?

A

It controls blood volume, salt balance and blood pressure

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13
Q

What drugs target the RAAS system?

A
  • Angiotensin receptor blockers (ARBs)

* Angiotensin Converting Enzyme inhibitors (ACEis)

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14
Q

What is Renin secreted by?

A

The kidney

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15
Q

What does Renin do?

A

It cleaves Angiotensinogen to Angiotensin I

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16
Q

What does ACE stand for?

A

Angiotensin Converting Enzyme

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17
Q

What does ACE do?

A

Cleaves Angiotensin I (ATI) to Angiotensin II (ATII)

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18
Q

What does ATII do?

A

It causes vasoconstriction of vascular smooth muscles and aldosterone release

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19
Q

What is Aldosterone?

A

A steroid hormone that promotes reabsorption of Na+ and H2O in the kidney increasing blood volume

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20
Q

Where does ATI come from?

A

The cleavage of Angiotensinogen by Renin

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21
Q

Where does ATII come from?

A

ACE converting ATI to ATII

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22
Q

What causes Aldosterone to be secreted?

A

ATII

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23
Q

Where is Aldosterone produced?

A

In the adrenal glands

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24
Q

What is the release of Renin stimulated by?

A

B1 activation due to low blood pressure

25
Q

What is the end goal of the RAAS system?

A

To increase blood volume and blood pressure

25
Q

What is the end goal of the RAAS system?

A

To increase blood volume and blood pressure

26
Q

How do beta 1 blockers reduce BP?

A

By reducing cardiac output and by decreasing renin secretion

27
Q

What is the signal pathway that increases release of Renin?

A

Adrenaline binds to B1 receptors activating Gs which activates AC and cAMP resulting of increased renin secretion

28
Q

How do B1 antagonists affect Renin secretion?

A

They will block B1 agonists from starting the Gs cascade suppressing renin secretion and RAAS system

29
Q

Where does ACE primarily exist?

A

In the pulmonary capillary endothelium as a membrane bound protein

30
Q

What receptor does ATII bind to?

A

The ATI receptor

31
Q

What kind of G receptors are ATI receptors that bind to ATII?

A

Gq receptors

32
Q

What are the two main target tissues of ATII?

A
  • The Adrenal cortex

* Vascular smooth muscle

33
Q

What does the Adrenal Cortex release?

A

Aldosterone

34
Q

What does ATII do the adrenal cortex and vascular smooth muscle?

A

Causes the release of aldosterone from the adrenal cortex and vasoconstriction of vascular smooth muscle

35
Q

What is the intracellular pathway that leads to release of Aldosterone in the adrenal glands?

A
  • ATII binds to ATI receptors which are Gq linked
  • Increased calcium binds to calmodulin
  • Calmodulin triggers synthesis and release of aldosterone
36
Q

What is the intracellular mechanism that ATII causes vasoconstriction?

A
  • ATII binds to ATI receptors which are Gq linked
  • Increased calcium binds to calmodulin
  • Calcium Calmodulin activates MLCK
  • MLCK which phosphorylates the MLC causing constriction of the muscles
37
Q

How is Aldosterone able to interact with its receptor and why?

A

Aldosterone must cross the plasma membrane to interact with its receptor because it is a steroid hormone

38
Q

What is the intracellular cascade that allows aldosterone to work?

A
  • Aldosterone crosses the membrane to bind with receptor
  • Receptor causes unbinding of chaperone protein
  • Translocates to the nucleus
  • Affects transcription of target genes
  • Generates mRNA and proteins
  • Leads to biological effects
39
Q

Which part of the kidney does Aldosterone target?

A

The Distal convoluted tubule

40
Q

Which three parts of the DCT does Aldosterone target?

A
  • Na+/K+ pump
  • Epithelial Na+ channel (ENaC)
  • NCC (Na+/Cl- symporter)
41
Q

What is the net effect of aldosterone?

A

To promote Na+ and therefore water reabsorption to increase BP

42
Q

What does NCC do?

A

Transports sodium into the epithelial cell of the nephron so that the sodium potassium exchange pump can pump sodium into the interstitium blood

43
Q

What does aldosterone do to the sodium transported in the DCT?

A

Causes them to be upregulated in order to increase water reabsorption

44
Q

What level does aldosterone, a steroid hormone act?

A

At the level of gene transcription

45
Q

What is the main ACE inhibitor drug?

A

Captopril

46
Q

What do ACE inhibitors do?

A

The prevent the cleavage of ATI to ATII

47
Q

What does the prevention of ATI converting to ATII by ace inhibitors do?

A

Prevent the Vasoconstriction and aldosterone secretion of ATII

48
Q

What is the most common side effect of ACE inhibitors and why?

A

Dry cough because ACE also causes the breakdown of bradykinin which causes bronchoconstriction

49
Q

What is the overall effect of ACE inhibitors?

A

By blocking Vasoconstriction and Aldosterone secretion it decreases BP

50
Q

What is the main ATI blocker (ARB)?

A

Losartan

51
Q

What binds to ATI receptors?

A

ATII

52
Q

What is the effect of ARBs?

A

They have a vasodilatory effect

53
Q

Why do ARBs have a vasodilatory effect?

A

Because they block the ATI receptors and don’t allow ATII to bind

54
Q

Why are ARBs better tolerated than ACE inhibitors?

A

Because they don’t have the dry cough side affect cause by bradykinin not being broken down

55
Q

What is the main Aldosterone Antagonists?

A

Spironolactone

56
Q

What is Spironolactone?

A

A competitive antagonist of the aldosterone receptor

57
Q

What do Aldosterone Antagonists do?

A

The prevent aldosterone receptors from being activated

58
Q

What are the effects of Aldosterone inhibitors?

A

They have diuretic actions be stopping the reabsorption of Na+

Pharm (31 decks)

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