presentation about beta blockers and the diuretics in treating hypertension

1. Beta Blockers And
Diuretics In
Treatment Of
Hypertension
The subject: Basic
pharmacology II
Subject professor: Dr. Mariam
Chipashvili
BY: Juma Awar
UG: 1802018

2. Beta Blockers
Mechanism and
Sites of Action
 Beta 1 selective: Atenolol,
Metoprolol, Esmolol
 Beta 1 and Beta 2 Non-
selective: Propranolol,
Timolol
 Alpha and Beta Blocker:
Labetalol, carvedilol
 β blockers are especially
useful in preventing the
reflex tachycardia that often
results from treatment with
direct vasodilators

3.  Propranolol: decreases blood pressure
primarily as a result of a decrease in
cardiac output. Inhibits the stimulation
of renin production by catecholamines.
 Propranolol can be administered twice
daily
 Toxicity: blockade of cardiac, vascular,
or bronchial β receptors (in patients
with bradycardia and in patients with
asthma).
 withdrawal syndrome
 Metoprolol & Atenolol: the most
widely used β blockers in the
treatment of hypertension.
 cardioselectivity is advantageous in
treating hypertensive patients who
also suffer from asthma or peripheral
vascular disease.
 cardioselectivity is not complete.
 Metoprolol is extensively metabolized
by CYP2D6, short half-life of 4–6 hours
 Atenolol is excreted primarily in the
urine with a half-life of 6 hours
 Patients with reduced renal function
should receive lower doses.

4.  Labetalol, Carvedilol, & Nebivolol:
These drugs have both β-blocking
and vasodilating effects
 Labetalol used to treat
hypertensive emergencies
 Carvedilol metabolized in the liver;
half-life is 7–10 hours
 Nebivolol is a β1-selective blocker
with vasodilating properties. half-
life is 10–12 hours.
 Esmolol is a β1-selective blocker
that is rapidly metabolized via
hydrolysis by red blood cell
esterases. short half-life (9–10
minutes). administered by
intravenous infusion.
 Esmolol is used for management of
intraoperative and postoperative
hypertension

5. Diuretics
Mechanism and
Sites of Action
 Thiazide diuretics are
appropriate for most
patients with mild or
moderate hypertension and
normal renal and cardiac
function.
 Chlorthalidone is likely to be
more effective than
hydrochlorothiazide because
it has a longer duration of
action.
 furosemide are necessary in
severe hypertension

6.  Thiazides inhibit NaCl transporter,
their action is predominantly in the
DCT.
 Thiazides are active by the oral
route and have a duration of action
of 6–12 h, considerably longer
than most loop diuretics.
 Chlorothiazide is s slowly absorbed
and has a longer duration of
action, not very lipid-soluble.
 promotes sodium-calcium
exchange at the basolateral
membrane.
 Toxicity: may blunt uric acid
secretion and elevate serum uric
acid level.
 Hypokalemic Metabolic Alkalosis
 Hyperglycemia
 Hyperlipidemia
 Allergic Reactions
 Loop diuretics selectively inhibit
NaCl reabsorption in the TAL. the
luminal Na+ /K+ /2Cl− transporter.
 loop diuretics cause an increase in
Mg2+ and Ca2+ excretion.
 They are eliminated by the kidney
by glomerular filtration and
tubular secretion.
 The duration of effect for
furosemide is usually 2–3 hours.
The effect of torsemide lasts 4–6
hours.
 use of the loop diuretics include
acute pulmonary edema and other
edematous conditions.
 Toxicity: Hypokalemic Metabolic
Alkalosis
 Hypomagnesemia
 Hyperuricemia
 Ototoxicity

7. THANK YOU