the use of ACEI , ARBS & Adrenergic receptor blockers in managing hypertension

1. By : Abeer ahmed
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2. hypertension pathology :
• The force of the blood is constantly putting pressure on the walls
of blood vessels this is known as “blood pressure”.
• Blood pressure is regulated by chemicals in the body that change
the diameter of the blood vessel depending on the needs of the
body through vasoconstriction or vasodilatation .

4. Untreated hypertension may cause :

6. Ace inhibitors :
• A chemical that is present on the wall of blood vessels called
angiotensin 1 binds to an enz called angiotensin converting enz (ACE).
• Angiotensin I in the blood is itself formed from angiotensinogen, a pro
tein produced by the liver and released into the blood
• once bound a new chemical called angiotensin 2 is created .
• Angiotensin 2 binds to receptors on the smooth muscles of the
blood vesseles leading them to narrow (vasoconstriction) .

7. Figure showing ace inhibitors “the pink one “ blocking the active site of
angiotensin converting enzyme .
This prevents the chemical converion of angiotensin 1 to angiotensin2 .

9. The following is a list of the ACE inhibitors :
• benazepril (Lotensin)
• captopril (Capoten)
• enalapril (Vasotec, Epaned)
• fosinopril (Monopril)
• lisinopril (Prinivil, Zestril)
• moexipril (Univasc)
• perindopril (Aceon)
• quinapril (Accupril)
• ramipril (Altace)
• trandolapril (Mavik)

10. What are the side effects of ACE inhibitors?
• ACE inhibitors usually are not prescribed for pregnant women bec
ause they may cause birth defects.
• Individuals with bilateral renal artery stenosis (narrowing of the
arteries that supply the kidneys) may experience worsening of
kidney function.
• It may take up to a month for coughing to subside, and if one
ACE inhibitor causes cough it is likely that the others will too.

11. • ACE inhibitors may increase blood levels of potassium and cause
hyperkalemia.
• ACE inhibitors also may increase the blood concentration of lithium .
• There have been reports that nonsteroidal anti-inflammatory drugs (N
SAIDS) may reduce the blood pressure lowering effects of ACE inhibit
ors.
• Patients receiving diuretics may experience excessive reduction in
blood pressure when ACE inhibitors are started. Stopping the diuretic or
increasing salt intake prior to taking the ACE inhibitor may prevent
excessive blood pressure reduction.

12. • ACE inhibitors should not be combined with ARBs because such
combinations increase the risk of hypotension, hyperkalemia, and
renal impairment.

14. Mechanism of interaction between diuretics and
ACEI
• Diuretics can reduce plasma volume leading to reduced
renal blood flow. This may lead to increased serum creatinine
concentrations.
• The kidney can compensate via the renin-angiotensin
system by constricting the efferent renal arteriole to increase
glomerular filtration pressure and favor water and sodium rete
ntion

15. Mechanism of NSAIDs interaction with ACEI
• NSAIDs, by inhibition of prostaglandins and bradykinin, prod
uce vasoconstriction of the afferent renal arteriole.

16. For what conditions are ACE inhibitors used?
• controlling acute and chronic high blood pressure
• treating left ventricular dysfunction and
heart failure.
• preventing strokes.
• preventing and treating kidney disease
(nephropathy) in people
with hypertension or diabetes.

18. ARBs mechanism of action
• angiotensin II receptor antagonists work By attaching
to AT1 receptors on smooth muscle cells lining the blood
vessels, this drug blocks angiotensin II from binding.

19. The following is a list of currently available ARBs:
• azilsartan (Edarbi)
• candesartan (Atacand),
• eprosartan (Teveten),
• irbesartan (Avapro),
• telmisartan (Micardis),
• valsartan (Diovan),
• losartan (Cozaar), and
• olmesartan (Benicar).

20. Adrenergic receptors :

22. Alpha-Adrenergic Blockers:
• Norepinephrine is released from the adrenal gland where
it circulates in the bloodstream and binds to proteins,
called alpha-adrenergic receptors, on the surface of smooth
muscles within the blood vessels.
• Once bound, the smooth muscle cells tighten, decreasing
the width of the blood vessel.

23. Alpha adrenergic blockers MOA :
• alpha-adrenergic blockers act By selectively attaching to al
pha-adrenergic receptors on smooth muscle cells lining th
e blood vessels, this drug blocks norepinephrine from bin
ding.

24. Examples of non-selective α-adrenergic recep
tor antagonists include:
• Phenoxybenzamine
• Phentolamine
• Tolazoline
• Trazodone
• Typical and atypical antipsychotics

25. Selective α1-adrenergic receptor antagonists include
• Alfuzosin
• Doxazosin
• Prazosin (inverse agonist)
• Tamsulosin
• Terazosin
• Silodosin[

26. Selective α2-adrenergic receptor antagonists
include :
• Atipamezole
• Idazoxan
• Mirtazapine
• Yohimbine
• carvedilol and labetalol are both α- and β-blockers.