This document discusses beta blockers and diuretics used in the treatment of hypertension. It describes the mechanisms and sites of action of various beta blockers including selective beta-1 blockers like atenolol and metoprolol, non-selective blockers like propranolol, and alpha-beta blockers like labetalol. It also discusses the pharmacokinetics and uses of specific beta blockers. The document then discusses thiazide and loop diuretics, their mechanisms of action in inhibiting sodium transport in the kidney, and their toxicities which can include hypokalemia, hyperglycemia, and hypomagnesemia.

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

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