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Unit 12
12.1
Pharmacology of HTN 1
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Jessica Jardine
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What is isolated systolic HTN?
Systolic >
140
Diastolic <
90
High
pulse pressure
Most
common
What is isolated diastolic HTN?
Systolic <
140
Diastolic >
90
Least
common
What is mixed HTN?
Systolic
>
140
Diastolic
>
90
What is the percentage of each HTN?
Essential
HTN >
90
%
Secondary
HTN <
10
%
What is essential HTN?
Idiopathic
HTN (
no clear causative factor
)
What is secondary HTN?
High
blood
pressure that is caused by an underlying medical
condition
or medication
renal
disorders
endocrine
disorders (primary hyperaldosteronism, phaechromocytoma, Cushing's syndrome)
drug-induced
(abuse (cocaine),
iatrogenic
(combined oral contraceptive, glucocorticoids))
pregnancy
- pre-eclampsia
What are the consequences of HTN?
Increased
risk of many CV disorders (
stroke
,
heart failure
,
peripheral arterial disease
,
CKD
etc.)
What are the mechanisms that underlie HTN?
Cardiac output
Peripheral resistance
Autonomic NS
Endothelium
Vasoactive peptides
RAAS
Arterial BP
=
CO
x
TPR
CO =
SV x HR
How does the autonomic NS impact HTN?
Heart
-
b1
receptor ->
increases
HR ->
increased
CO
Vessels
-
a1
receptor ->
vasoconstriction
,
b2
receptor ->
vasodilation
Short-term
regulation (e.g.
baroreceptor
reflex)
What do endothelial cells produce?
Vasoactive
agents (NO, PGI2, endothelin)
What is the effect of NO?
Vasodilation
by binding to
guanylyl cyclase
-> increase
cGMP
-> increase
PKG
-> smooth muscle
relaxation
What does prostacyclin (PGI1) do?
Vasodilation
What does enothelin do?
Vasoconstriction
Give 3 examples of vasoactive peptides.
Bradykinin
Natriuretic
peptides (
A
,
B
&
C
)
Vasopressin
(
ADH
)
What is the effect of bradykinin?
Vasodilation
ACE inhibtors
block
bradykinin inactivation
What is the effect of vasopressin (ADH)?
Vasoconstriction
What is renin produced by?
Juxtaglomerular
cells
RAAS is a target for many important &
effective drugs
used to treat HTN.
What is Liddle syndrome?
Rare
autosomal dominant
disorder that causes severe
HTN
at an
early
age
Caused by
mutations
in
beta
&
gamma
subunits of
ENaCs
-> prevents
channel internalisation
&
degradation
->
overexpression
of
ENaCs
->
excess Na+ reabsorption
What is the treatment of
Liddle syndrome
?

ENaC channel blockers
(e.g.
amiloride
)
Fill in the blanks
A)
peptides
B)
receptors
C)
AT-II
D)
AT1
4
Different classes of drugs used to treat HTN?
Diuretics
Renin
inhibitor (-kiren)
ACE
inhibitor (-pril)
Angiotensin Receptor Blocker
(ARB) (-sartan)
Ca
+
2 channel
blocker (-dipine)
Beta
blockers (-lol)
Centrally
acting
a2 agonists
Vasodilators
What is Stage 1 HTN?
140
/
90
<
ABP
<
159
/
99
What is Stage 2 HTN?
160
/
100
<
ABP
<
180
/
120
What is Stage 3 HTN?
SBP
>
180
OR
DBP
>
120
What do natriuretic peptides do?
Increase
Na+
&
water excretion
(in urine)
What is hexamethonium?
Analogue of ACh
Target:
nicotinic
receptor
Activity:
channel blocker
Blocks
sympathetic
&
parasympathetic
NS
What are the functions of voltage-gated Ca+2 channels?
Cardiac
AP/pacemaker
Smooth
/skeletal muscle contraction
Endocrine
(e.g. insulin secretion)
Ntr
release