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Unit 12 Week 1 (Sam) > Pharmacology of hypertension > Flashcards

Pharmacology of hypertension Flashcards

1
Q

What is hypertension

A

persistently raised arterial blood pressure

140/90

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2
Q

normal blood pressure

A

120/80

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3
Q

elevated blood rpessure

A

120-129/ <80

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4
Q

hypertension stage 1

A

130-139/ 80-89

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5
Q

hypertension stage 2

A

140+/ 90+

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6
Q

hypertension stage 3

A

180+/ 120+

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7
Q

What does clinical management depend on

A

severity and cause

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8
Q

2 typoes pf hypertension cause

A

essential (>90%)

secondary

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9
Q

essential hypertension

A

cause is unknown (idiopathic)

no clear causative factor

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10
Q

secondary hypertension

A
  • renal disorders (role of kidneys in regulating long term BV and therefore BP)
  • Endocrine: 1* hyperaldosteronism (fluid regulation)

phaeochromocytoma (sympathetic NS)

Cushing’s syndrome (cortisol)

  • Drug induced- abuse- e.g., cocaine (SNS)
  • iatrogenic e.g., combined oral contraceptive
  • pregnancy- pre-eclampsia
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11
Q

exogenous causes of hypertension

A

smoking

diet

stress

drugs

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12
Q

endogenous (genetic) causes of hypertensino

A

obesity

ethnicity

metabolic/ hormonal

renal (RAAS)

CNS

arterial

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13
Q

Consequences of hypertension

A

inc reased risk of cardiovacular disorder

coronary artery disease

stroke

heart failure

peripheral arterial disease

vascualr dementia

chronic kidney failure

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14
Q

pathophysiology mechanisms involved

A
  • Cardiac output
  • Peripheral resistance
  • Autonomic nervous system
  • Endothelium
  • Vasoactive peptides
  • Renin-angiotensinogen-aldosterone system
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15
Q

lowering ypertension affects health how?

A

health benefits

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16
Q

ABP=

A

CO x TPR

ABP = force on walls

CO= flow of blood

TPR= resistance of vessels to flow

force = flow x resistance

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17
Q

to reduce ABP you

A

decrease either CO or TPR or both

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18
Q

Cardiac output =

A

stroke volume x HR

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19
Q

stroke volume is directly proportional to

A

central venous pressure

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20
Q

paheachromocytoma

A

benign tumour in adrenal gland

increase adrenaline

increase CVP

responsive vasoconstriction

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21
Q

in most eddential hypertension which of CO and TPR is raised

A

TPR

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22
Q

chronic adaptive response in blood vessels may lead to

A

irreversible rise in TPR

23
Q

Role of autonomic NS in hypertension

A

heart function (CO)

vessel function (TPR)

SR regulation of pressure and flow: baroreceptor reflex and myogenic response

sympatholytic (antag or inhib SNS transmission) drugs lower ABP

24
Q

Which receptors does adrenaline act upon to cause vessel smooth muscle constriction- vasoconstriction

A

A2 adrenoreceptor

25
Q

ANS heart function

A

B1 receptors-activation by catecholamines increases sinoatrial (SA) nodal, atrioventricular (AV) nodal, and ventricular muscular firing, thus increasing heart rate and contractility. incvreases CO

vessel function- arteriolar tone regulates TPR and venous tone CVP

a1- vasoconstriction

B2- vasodilation

26
Q

endothelium

A
  • Endothelial cells produce vasoactive agents
  • EDRF (endothelium-derived relaxing fibre) = Nitric oxide (NO) -vasodilator
  • prostacyclin - vasodilator

andelyl cyclase- increase cGMP- increase PKG sm. muscle relaxation

endothelin- vasoconstrictor

atheroma (plaque) decreases NO production- constrict

27
Q

vasoactive peptides

A

bradykinin- vasodilator (ACE inhibs stop bradykin inactivation- keeping dilated)

Natriuretic peptides-direct vasodilators —–NPR1 (receptor) = guanylyl cyclase = increased cGMP = sm muscle relaxation

+ increase sodium and water excretion- secreasing blood volume

ADH= vasoconstrictor, increases BP and H20 reabsorption

28
Q

natriuretic peptides

A

ANP-atrial: secreted by atrium

BNP- brain: secreted by ventricles

CNP- C-type

secreted in response to low BP

29
Q

link between vasodilation and BP

A

vasodilation

increase venous capacitance

decrease central venous oressure

decreases ventricular preload

decreases CO

30
Q

Renin-angiotensin-aldosterone system in BP

A

longer term regulation of BV (ECF) and systemic vascular resistance

RAAS is a target for many important and effective drugs used in hypertension

31
Q

ABp and renin

A

decrease in BP→ increase Symp. activity and decrease GFR

a) increase symp- activates B1 receptors on granular cells of JGA- release of renin
b) macula densa cells detect Na+/Cl- in DCT– decrease GFR – decrease NaCl filtered load– release renin– dailtion of AFF and constriction of EFF– less water is lost through filtration– more in vessels

32
Q

angiotensinogen

A

plasma protein produced by liver and secreted into blood

the substrate for renin

gtes converted into ang1

33
Q

angiotensin 1

A

endogenous peptide

decapeptide cleaved from N-terminal of ang by renin

converted to ang II by ACE. ACE is widely expressed e.g., lung

34
Q

angiotensin II

A

octapeptide produced by cleavahe of C terminal dipeptide by ACE

full agonist at AT1 receptor (GCPR) causing the release of aldosterone (mineralocorticoid) from adrenal cortex- increasinf ECF

arteriolar vasoconstrictor

causes ADH release from posterior pituituary

35
Q

how many ACE enzymes are there

A

2

ACE 1

ACE 2

36
Q

ACE 1

A

widely expressed in endothelium of lungs and kidneys

has 2 catalytic ZN metalloproteinase domains

cleaves AT-1 - AT-2

also cleaves bradykinin, stopping its vasodilatory effects

37
Q

ACE 2

A

1 catalytic domain

cleaves ANG-II antagonising it

38
Q

AT1 (angiotensin II type 1 receptor)

A

PGCR (Gi and Gq signalling)

activated by anG ii

Causes:

sm. muscle contraction and vasoconstriction

C and SNS stimulation

aldosterone release

ADH release

tubular Na+ reabsorption in the PCT

endothelin release (vasoconstictor)

39
Q

Aldosterone

A

steroid (mineralocorticoid)

full agonist at intracellular mineralocorticoid receptors in tubular cells of the DCT

activation causes na+reuptake

40
Q

mineralocorticoid receptor

A

nuclear hormone receptor

Expressed in epithelia with high electrical resistance, e.g. distal kidney tubular cells

selectively changes transcription of cell– increasing production of ENaCs and Na+/ K+-ATPase pump

41
Q

spirinalactone

A

competitive antagonist of mineralocorticoid receptor

42
Q

epithelial soidium channels )ENaCs

A

widely expressed esp in kidney tubules (late DCT and CD) , lung and resp tract

increased ENaC expression on apical membrane due to activation of mineralocorticoid receptor increases Na+ permeability and Na+ reabsorption from tubule lumen into the cell

rate limiting step in salt reabsorption in this part of the nephron

these are NOT voltage gated

43
Q

amiloride is a what

A

ENaC blocker potassium sparing

44
Q

Na+Cl- ATPase (Na+ pump)

A

tansmembrane ATP-dependant active transporter

ubiquitously expressed

for each ATP, 3 Na+ out and 2k+ in

pumps Na+ out of cell into interstitium, keeping intracellular conc low so the NaKATPase pump can keep working

45
Q

what drugs inhibit Na+Cl-ATPase pumps

A

cardiac glycosides e.g., digoxin

46
Q

Liddle syndrome

A

rare genetic (autosomal dominant) disorder

causes severe hypertension from a young age

mutations prevent channel internalization and degradation

overexpression of ENaCs causes excess Na+ reabsorption

treat with ENaC blockers e.g., amiloride

47
Q

Master slide

A
48
Q

antihypertensive drugs

A

diURETICS (thiazides, loops, K sparing)

renin inhibitor

ACE inhibitos -pril

Angiotensin recptor blocker -sartan

B blockers -lol

calcium channel blockers -dipine

centrally acting a2 agonists e.g., clonidine

vasodilators

49
Q

aliskiren

A

renin inhibitor

essential hypertension

target= renin action= competitive inhibitor

physiology: decrease production of AngI

50
Q

enalapril

A

ACE inhibitor (most ACE inhibitors are pro drugs)

Prodrug

essential hypertension and heart failure

target: ACE Activity: competitive inhibitor

Physiology: decrease prod of AT-II and decrease breakdown of the vasodilator bradykinin

51
Q

valsartan

A

angiotensin receptor blocker

essential hypertension + heart failure

target: AT1. activity: competitive antagonist

Physiology: decreases effects of AT-II…… no effect on bradykinin so no cough

52
Q

atenolol

A

selective B1 blocker

essential hypertension - angina -arrthmias

target: B1 receptor as higher affinity than B2. activity: competitive antagonist

Gs coupled therefore antagonism of their activation reduces activity of adenylyl cyclase and its downstream signalling via cyclic adenosime monophosphate and protein kinase A (PKA)

not understood but decreases CO, alters baroreceptor reflexes and decreases renin secretion

53
Q

amlodipine

A

calcium channel blocker

essential hypertension angina

target= L-type voltage gated calcium channel activity- gating inhibitor

greater specificity fpr sm over cardiac msucle

decreased calcium mobilisation in smooth muscle means vasodilation

54
Q

voltage gated calcium channels

A

all open in response to depolarisation

L-type: once open stay open for a Long time, inactivate slowly

phosphorylated by action of adrenaline/ NA

amlodipine does not block but stabillises it in either

1) an unresponsive state
2) a hyper-responsive state

Unit 12 Week 1 (Sam) (6 decks)

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