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Class
Hydrochlorothiazide
(HCTZ) Thiazide
diuretics
Loop diuretics
Drug (trade names)
Chlorothiazide
(Diuril)
chlorthalidone
(generic)
hydrochlorothiazide
(Microzide,
HydroDIURIL†)
polythiazide
(Renese)
Indapamide (Lozol†)
metolazone
(Mykrox)
metolazone
(Zaroxolyn)
bumetanide
(Bumex†)
furosemide (Lasix†)
torsemide
(Demadex†)
Mechanism of action
K-depleting: mechanism: By definition potassium-depleting
diuretics increase potassium excretion and, in practice,
they also usually deplete blood levels of magnesium. In
turn, the drug-induced magnesium deficiency can
contribute to further potassium depletion. Ultimately the
relationship between these two patterns of depletion can
be difficult to determine.
Mechanism: The loop diuretics inhibit sodium reabsorption
in the ascend-ing portion of the loop of Henle. Because this
portion of the nephron is responsible for reclaiming 3040% of the filtered sodium, inhibition at this site can result
in a very large diuresis. The loop agents are therefore the
most efficacious of all the diuretics. As with the thiazides,
the increase in the sodium appearing downstream in the
collecting duct results in an increase in the excretion of
potassium and hydrogen ion, and a hypokalemic metabolic
alkalosis may result. The loop agents also increase calcium
excretion.
Drug: take furosemide on empty stomach- food ↓ food
bioavailability, but may take w/ food/milk if GI distress
occurs
Potassium-sparing
diuretics
Aldosterone receptor
blockers
BBs
amiloride
(Midamor†)
triamterene
(Dyrenium)
Diet: ↑ K, ↑ Mg ( K/Mg supplement), ↓ cal, ↓ Na may be
recommended
Mechanisms Potassium is normally secreted in the
collecting ducts of the kidney, under the control of
aldosterone and in proportion to the amount of sodium
appearing in the lumen at this level. The aldosterone level
is increased when there is a net sodium loss or a decrease
in the "effective circulating blood volume." Most diuretics
increase the amount of potassium excreted because they
present more sodium to thecollecting ducts and increase
the circulating aldosterone level. The potassium-sparing
agents effectively reduce sodium reabsorption in this part
of the tubule and thereby reduce potassium excretion.
* Sodium transport inhibitors: Amiloride and triamterene
block a channel necessary for sodium reabsorption in the
collecting duct. Amiloride may also have an inhibitory
effect on Na,K-ATPase in this part of the tubule.
eplerenone (Inspra)
Aldosterone inhibition: Spironolactone is a direct
spironolactone
aldosterone receptor antagonist in the cells of the
(Aldactone†)
collecting duct of the nephron and modifies protein
synthesis as a result. Spironolactone also has other
endocrine effects, including an antiandrogenic action.
atenolol (Tenormin†) Mechanism of action: Beta blockers are competitive
betaxolol (Kerlone†) inhibitors and interfere with the action of stimulating
bisoprolol (Zebeta†) hormones on beta-adrenergic receptors in the nervous
metoprolol
system. Beta blockers can be subdivided into two distinct
(Lopressor†)
groups, known as beta 1 and beta 2. Beta 1 blockers mainly
metoprolol extended affect the heart; beta 2 blockers mainly affect receptors in
release (Toprol XL)
bronchial tissue
nadolol (Corgard†)
propranolol
(Inderal†)
propranolol longacting (Inderal LA†)
timolol (Blocadren†)
ACEIs
benazepril
(Lotensin†)
captopril (Capoten†)
enalapril (Vasotec†)
fosinopril (Monopril)
lisinopril (Prinivil,
Zestril†)
moexipril (Univasc)
perindopril (Aceon)
quinapril (Accupril)
ramipril (Altace)
trandolapril (Mavik)
Angiotensin-Converting Enzyme (ACE) is an enzyme in the
body which is important for the formation of angiotensin II.
The function of angiotensin II is to cause constriction of
arteries, thereby elevating blood pressure. ACE inhibitors
lower blood pressure by inhibiting the formation of
angiotensin II, thus relaxing the arteries. Relaxing the
arteries not only lowers blood pressure, but also improves
the pumping efficiency of a failing heart and improves
cardiac output in patients with heart failure.
Angiotensin II
antagonists
candesartan
(Atacand)
eprosartan (Teveten)
irbesartan (Avapro)
losartan (Cozaar)
olmesartan (Benicar)
The final active messenger of the renin-angiotensin
pathway is angiotensin II. Angiotensin II binds to AT1
receptors to cause vasoconstriction and fluid retention,
both of which lead to an increase in blood pressure. The
angiotensin II receptor blockers lower blood pressure by
blocking the AT1 receptors. Therefore they have similar
telmisartan
(Micardis)
valsartan (Diovan)
effects to angiotensin converting enzyme (ACE) inhibitors,
which inhibit the synthesis of angiotensin II by ACE.
However, non-ACE pathways can produce some
angiotensin II. ACE inhibitors also decrease bradykinin
breakdown and this action could be involved in some of
the beneficial and adverse effects of that class of drugs.
Therefore, a potential for differential clinical effects exists
for these two classes of drugs.