Vol. 117 No.

6 June 2014

Nonsteroidal anti-inflammatory drugs and antihypertensives:

how do they relate?
Zovinar Der Khatchadourian, DDS,a,* Isabel Moreno-Hay, DDS, PhD,b,* and Reny de Leeuw, DDS, PhD, MPHc
McGill University, Montreal, Quebec, Canada; University of Kentucky, Lexington, KY, USA

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely available as over-the-counter medications, despite their
numerous side effects and drug interactions. The aim of this article is to increase awareness of the hypertensive potential of
NSAIDs and their interference with antihypertensives. Patients with hypertension appear to be more susceptible than
normotensive individuals to the blood pressureeincreasing effect of NSAIDs. Most studies have found that short-term use of
NSAIDs does not pose a major risk for hypertension or increase in cardiovascular disease in healthy individuals. The calcium
channel blockers and b-blockers seem to be least affected by the concomitant use of NSAIDs. A dentist must weigh the
benefits and disadvantages of using NSAIDs in patients taking antihypertensive drugs. For those who may be at greater risk,
such as patients with hypertension and the elderly, careful selection of the class of NSAID and close monitoring are
appropriate measures, especially if long-term use is anticipated. (Oral Surg Oral Med Oral Pathol Oral Radiol 2014;117:
697-703)

Nonsteroidal anti-inflammatory drugs (NSAIDs) are
widely available as over-the-counter medications in
drugstores and supermarkets not only in the United
States but also worldwide. In 2010, an estimated US
$1.1 billion were spent on nonnarcotic analgesic drugs
in the United States.1
NSAIDs are very commonly used medications
despite their numerous side effects and drug in-
teractions. For instance, the acute administration of
NSAIDs has been associated with serious adverse
outcomes, such as allergic reactions, renal failure,
coagulation problems, and worsening of asthma.
Furthermore, the long-term administration of NSAIDs
can cause serious gastrointestinal (GI) adverse effects
(e.g., bleeding, ulcers), renal failure, and congestive
heart failure.2-4 Minor side effects, such as nausea,
dizziness, or gastric irritation, have also been reported.4-6
Several studies have found that the risk for complica-
tions increases in susceptible patients, for example
those who present with a history of ulcers, cardiovas-
cular disease, diabetes, or renal complications.7,8 The
risk of deleterious effects with NSAID use is increased
in the elderly population,4,5,9 yet Seager and Hawkey9
found in their study that over half of 24 million NSAID
prescriptions written in a year in the United Kingdom
were prescribed to the elderly population. Owing to the
*These authors have equally contributed to the article.
a
Faculty Lecturer, Montreal General Hospital, Faculty of Dentistry,
McGill University.
b
Resident, Orofacial Pain Center, College of Dentistry, University of
Kentucky.
c
Professor and Chief, Division of Orofacial Pain, University of
Kentucky.
Received for publication Jul 30, 2013; returned for revision Feb 4,
2014; accepted for publication Feb 21, 2014.
Ó 2014 Elsevier Inc. All rights reserved.
2212-4403/$ - see front matter
http://dx.doi.org/10.1016/j.oooo.2014.02.028
deleterious effects of NSAIDs, Seager and Hawkey9
debated whether NSAIDs should be prescribed to
manage conditions that are not life-threatening. Often
overlooked is the fact that long-term use of NSAIDs
can cause hypertension.10
NSAIDs also have numerous drug interactions. For
instance, most NSAIDs affect platelet function, leading
to increased risk of bleeding, when administered with
other drugs that impair hemostasis, such as warfarin and
selective serotonin reuptake inhibitors. NSAIDs also
displace many other drugs, including warfarin and an-
ticonvulsants, from albumin, thus leading to increased
risk of bleeding and potentially toxic levels of the dis-
placed drugs. Other oftenoverlooked interactions of
NSAIDs follow from their reduction of the renal so-
dium excretion and inhibition of prostaglandin (PG)
synthesis. These actions attenuate the effects of several
classes of antihypertensive medications.11,12
The aim of this article is to increase awareness of the
blood pressure (BP)eincreasing potential of NSAIDs
and their interference with antihypertensives. First we
provide an overview of the prevalence of hypertension
and the effect it may have on cardiovascular disease
(CVD). We then discuss the mechanisms of action of
NSAIDs, with emphasis on their potential to increase BP.
Finally, we discuss the most common antihypertensive
medications and describe how NSAIDs may interfere
with their actions.
Statement of Clinical Relevance
Dentists should be aware that NSAIDS can increase
blood pressure, especially in patients with hyperten-
sion. In addition, NSAIDs can interfere with the blood
pressureelowering mechanisms of antihypertensives.

697
ORAL MEDICINE
698 Khatchadourian, Moreno-Hay and de Leeuw
PREVALENCE AND IMPLICATIONS OF
HYPERTENSION
Hypertension is one of the known factors implicated in
CVD, such as stroke, coronary heart disease, and heart
failure,13,14 as well as in renal and ocular disease.14 Ac-
cording to the recently published Joint National Com-
mittee (JNC-8) recommendations for the management of
high BP in adult populations, hypertension is defined as
an average BP
140/90 mm Hg in the general population
younger than 60 years, whereas in patients older than 60
years, BP
150/90 mm Hg is defined as hypertension15;
for those with diabetes or chronic kidney disease, the
recommended BP is  130/80 mm Hg.16 Hypertension
is very common in the United States, affecting over 65
million adults.17 The American Heart Association esti-
mates that 25% of the overall population, and 55% to
60% of those aged between 65 and 74 years, have hy-
pertension.18 A study based on the NHANES database
(National Health and Nutrition Examination Survey)
performed in 2003 and 2004 found that 24.3% of the
hypertensive population was unaware of their condition,
and of those that were aware, only 53.7% were receiving
proper treatment.19 Thus, over 60% of adults with hy-
pertension living in the United States have uncontrolled
hypertension and thus are at risk for CVD complications.
Both transient and sustained elevations in BP are risk
factors for cardiovascular mortality and morbidity.20 For
instance, an increase of 5 mm Hg in the diastolic BP
(DBP) can increase the risk of stroke by 67% and the risk
of events associated with coronary heart disease by
15%.21 From a meta-analysis of 61 randomized controlled
trials involving over 1 million participants,22 it was
concluded that for every incremental increase of 20 mm
Hg in systolic BP (SBP) and 10 mm Hg in DBP, starting
with a BP of 115/75 mm Hg, the risk of CVD doubled.
Randomized controlled trials have also found that
lowering SBP by 10 mm Hg (and 5 mm Hg for DBP) can
reduce the risk of stroke by 40% and that of ischemic heart
disease by 30%.23-25 Even smaller reductions in BP can
have a positive effect.18,22 Pain can also increase BP.26
MECHANISM OF ACTION OF PGs
PGs are produced through oxygenation of arachidonic
acid by cyclooxygenase (COX).27,28 There are 2 vari-
eties (isoenzymes) of the COX enzyme: COX-1 and
COX-2. COX-1 is constitutive and present in most
normal tissues, whereas COX-2 is inducible during
inflammatory processes but is constitutive to the brain
and kidneys. The constitutive COX-1 enzyme plays a
key role in the integrity of the GI mucosal barrier, in
kidney function, in maintenance of the vascular tone,
and in platelet function.
PGs have many physiologic actions in the brain, the
GI tract, the kidneys, and the cardiovascular system.
They also play a role in bone resorption, pain, and
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June 2014
inflammatory responses.29 The effects of PGs on the
kidneys and cardiovascular system are most important
for this review and are described in more detail than the
other physiologic effects.
In the central nervous system, prostaglandin E2
(PGE2) is involved in fever generation and stimulates
the secretion of adrenocorticotropic hormone. It has
been proposed as a sleep inducer.29 In the GI tract, PGs
regulate secretion of mucus and affect GI motility. In
renal function, PGs are responsible for the modulation
of blood circulation and of salt and water excretion.
Solute homeostasis is maintained in part by PGs, such
as PGE2, which decreases the sodium resorption. In the
cardiovascular system, PGs regulate BP by modulating
the renin-angiotensin system (RAS). Renin is an
enzyme secreted by juxtaglomerular cells; it is
responsible for converting angiotensin I into angio-
tensin II. PGI2 stimulates the release of renin and
therefore the production of angiotensin II, which has a
potent vasoconstrictor effect leading to an increase in
BP. In addition, angiotensin II also promotes the pro-
duction of aldosterone from the adrenal cortex. Aldo-
sterone is a steroid hormone that acts on the nephron
and elevates BP by water and sodium reabsorption and
potassium secretion.30 PGs further contribute to the
regulation of the cardiovascular system by eliciting the
contractile (PGI2) and relaxing (thromboxane A2
[TxA2]) vascular smooth muscles and by inhibiting
(PGI2) or inducing (TxA2) platelet activation and ag-
gregation. It has been proposed that the balance of the
PGI2 and TxA2 systems is important for maintaining
vascular homeostasis.29,31 PGs are involved in the in-
flammatory process along with other mediators, such as
histamine and bradykinin, which are responsible for
vascular permeability and edema. Furthermore, PGs are
also believed to sensitize the free endings of sensory
neurons, inducing hyperalgesic responses in the pe-
riphery.29 Different side effects will be produced by the
selective or nonselective inhibition of the COX en-
zymes and thus production of PGs.32
MECHANISM OF ACTION OF NSAIDs
The main mechanism of action by which NSAIDs exert
their effect is by means of inhibiting the COX enzyme,
thus inhibiting the production of PGs. The analgesic
and anti-inflammatory effects of NSAIDs are based on
the inhibition of PGs. NSAIDs may thus affect all of the
aforementioned systems. There are several proposed
mechanisms by which NSAIDs, by virtue of their ac-
tions on some of these systems, could raise BP.
Sodium and fluid retention
PGs are released to promote vasodilation and enhance
renal blood flow. By blocking the tubular PGE2,
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Volume 117, Number 6
NSAIDs promote sodium and fluid retention, increasing
the tubular reabsorption of sodium, which may lead to
an increase in BP.30,33,34 It appears that sodium reten-
tion is mostly mediated by COX-2.31,34
Renin-angiotensin system
In some cases, NSAIDs may reduce BP by inhibiting
the production of renin released by PG. This hypoten-
sive effect is due to the combination of 2 processes.
First of all, the aldosterone released by PGs causes
increased sodium and water reabsorption and excretion
of potassium, thereby increasing BP. In addition, the
RAS also regulates the secretion of antidiuretic hor-
mone. Experimental studies, under well-controlled
conditions, have found selective inhibition of COX-2 to
inhibit the RAS and reduce hypertension.34
Moreover, the hyporeninemia and hypoaldosteron-
ism induced by NSAIDs may manifest as hypercalce-
mia due to a decrease in potassium excretion. This
hypercalcemia can cause cardiac arrhythmias.30 Arm-
strong and Malone35 proposed that this hypercalcemic
condition, although infrequent, may contribute to hy-
pertension independently of hemodynamic and elec-
trolyte balance.
Inhibition of PG vasodilation
NSAIDs may increase the BP by a direct effect on
vascular smooth muscle.36 PGI2 is synthesized by
prostacyclin synthase and has vasodilatory effects. The
administration of NSAIDs inhibits COX-2 production
of PGI2, resulting in an increase in peripheral resis-
tance34 responsible for BP increase. Animal model
studies found that the infusion of PGE2 evoked hypo-
tension in mice. Interestingly, PGE2 was produced and
increased in urinary secretion when animals were fed a
high-salt diet, possibly to downregulate the BP.29
Cytochrome P-450-dependent monooxygenase
system
By inhibition of COX enzymes, the metabolism of the
arachidonic acid is forced through alternative pathways.
Examples are the lipoxygenase and P-450 cytochrome
nicotinamide adenine dinucleotide phosphateedependent
monooxygenase pathways. In recent years, it has been
found that the metabolism of arachidonic acid by
cytochrome P-450 results in the production of metab-
olites with potential effects on raising BP.33,34 Animal
studies have found that the metabolites epoxyeicosa-
trienoic acid, hydroxyeicosatetraenoic acid, and 20-
carboxyl arachidonic acid, produced through this
“third” pathway, are involved in the pathogenesis of
hypertension by modification of renal function. How-
ever, data for humans in this regard are limited.37
REVIEW ARTICLE
Khatchadourian, Moreno-Hay and de Leeuw 699
Given the aforementioned factors, it should be clear
that the use of NSAIDs may raise the BP in some in-
dividuals, mostly through their action on PGs. Gaz-
iano36 found that the acute effect of NSAIDs appears to
cause a slight short-term increase in BP and that this is
likely to be reversible. However, the effect on chronic
hypertension due to the deleterious effects on the kid-
neys induced by the long-term use of NSAIDs is not
clear and requires further research.36
A meta-analysis38 published in 2009 compared the
effects of different types of NSAIDs on BP, and the
authors found that a few selective COX-2 inhibitors
were associated with an elevation in BP compared with
placebo or nonselective NSAIDs.38 However, these
selective COX-2 inhibitors are no longer on the market.
The meta-analysis,38 along with other recent
studies,39,40 found no differences in the incidence of
hypertension between celecoxib and nonselective
NSAIDs. However, a long-term study found that pa-
tients treated with celecoxib, 200 mg or 400 mg, for the
prevention of colorectal adenomas had an increase in
the SBP of 2 mm Hg and 2.9 mm Hg, respectively, after
1 year and 2.6 mm Hg and 5.2 mm Hg, respectively,
after 3 years. These results indicate a dose-dependent
and possibly increasing rise of BP with the long-term
use of such medications.41
Patients with hypertension appear to be more sus-
ceptible than normotensive participants to the BP-
increasing effect of NSAIDs. A systematic review
found an increase of þ1.1 mm Hg BP in normotensive
participants taking NSAIDs. In patients with controlled
hypertension, the increases were variable, ranging up
to þ14.3 mm Hg for SBP and þ2.3 mm Hg for DBP.33
Among the various nonselective NSAIDs, indometh-
acin, naproxen, and piroxicam were associated with the
greatest increase in BP in the hypertensive popula-
tion.33 A review article by Morgan and Anderson
concluded that salt-sensitive patients with hypertension
were more likely to be affected by the use of NSAIDs.42
Frishman34 concluded that the incidence for increased
BP related to NSAIDs intake was low and that increases
were usually less than 5 mm Hg. However, he stated
that certain patients are at a higher risk for BP increase
with concomitant use of NSAIDs, such as patients with
hypertension, those treated with antihypertensives,
those with a history of cardiovascular disease, or those
with renal or liver disease.34
MECHANISM OF ACTION OF
ANTIHYPERTENSIVE MEDICATIONS
BP is regulated through 3 separate mechanisms: by
baroreflexes that are mediated by the sympathetic ner-
vous system (SNS), by inflammatory mediators, and by
the RAS.43 These mechanisms can affect BP on their
own as well as in synchrony with each other, depending
ORAL MEDICINE
700 Khatchadourian, Moreno-Hay and de Leeuw
on the level of BP fluctuations. The baroreflexes are
activated when the BP is decreased beyond a certain
level, which results in the SNS increasing cardiac
output and peripheral vascular resistance to counteract
the reduced BP. Inflammatory cytokines will cause
vasodilatation, leading to edema of tissues and
decreased BP. The RAS regulates BP through water
and sodium reabsorption and secretion of antidiuretic
hormone. The effect of NSAIDs on the RAS is
responsible for an increase in total peripheral resistance,
and this negates the BP-reducing effect of all antihy-
pertensive medications in a general fashion.
INTERACTION OF ANTIHYPERTENSIVES WITH
NSAIDs
In addition to raising the BP by themselves, NSAIDs
can also negate the BP-lowering effects of many med-
ications used to treat hypertension, again mostly by
counteracting the PG effect of such medications. There
are different modalities for the treatment of hyperten-
sion. Nonpharmacologic therapy includes lifestyle
changes to promote weight loss (through diet and ex-
ercise) and to promote healthy dietary changes,
including reduction in caffeine, sodium, fat, and alcohol
intake and increase in fruit, fish, lean protein, and fiber
intake.27,28 Another therapy for hypertension is phar-
macotherapy.44 Antihypertensives are widely pre-
scribed in the United States and elsewhere, with an
estimated cost of more than US $8 million in the United
States, based on a 2001 study performed by Hodgson
and Cai.45 There are 5 major different classes of anti-
hypertensives: (1) diuretics; (2) those affecting the
RAS, such as the angiotensin-converting enzyme in-
hibitors (ACEIs), angiotensin receptor blockers
(ARBs), and renin inhibitors; (3) vasodilators; (4)
sympatholytic agents; and (5) other cardiovascular
affecting medications, such as b-blockers and calcium-
channel blockers.46 Often, hypertension is controlled
using multiple antihypertensive agents at the same time.
Each agent will decrease BP through one or more
mechanisms. The JNC-8 recommends as first-line
treatment the following classes of medications: thia-
zide-type diuretics, ACEIs, ARBs, and calcium channel
blockers. It recommends further that medication classes
such as the a-blockers and b-blockers, the aldosterone
antagonists, and the loop diuretics should only be
considered as later-in-line alternatives.15
Diuretics
This class of antihypertensive medication is subdivided
into several classes; the loop and thiazide-type diuretics
are 2 major classes commonly prescribed to treat hyper-
tension.18 The loop diuretics inhibit sodium reabsorption
at the level of the loop of Henle by competing with
chloride for the sodium/potassium cotransporter,
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June 2014
consequently inhibiting sodium and chloride reabsorp-
tion. Loop diuretics can also stimulate renal PG synthesis,
particularly of PGE2, which is a vasodilator. Thus, the
NSAIDs, by virtue of blocking renal PGE2 synthesis, will
increase sodium reabsorption and reduce the effect of
loop diuretics. The thiazide-type diuretics exert their ef-
fect in the distal convoluted tubule, where the reabsorp-
tion of sodium and chloride is inhibited. These agents also
reduce calcium and uric acid excretion. Hyperreninemia
and hypoaldosteronism induced by NSAIDs can negate
the effect of diuretics,18,35 possibly owing to resulting
hyperkalemia. Another category of diuretics prescribed
for hypertension is the potassium-sparing family. In this
group of antihypertensives, one subclass acts as
competitive antagonist of aldosterone, whereas another
one is independent of aldosterone function. The first
subclass can be affected by NSAIDs’ effect at the RAS
level. The second subclass, usually used in combination
with thiazide diuretics, can increase renal vascular resis-
tance; thus combination of this potassium-sparing diuretic
with NSAIDs can result in acute renal failure lasting for
several days associated with secretion of PGE2.47
Angiotensin systemeaffecting agents
Angiotensin II increases BP in several ways: through
the aldosterone system, by increasing the response to
catecholamines, and by causing vasoconstriction
mediated by release of PGE2.48 Angiotensin-converting
enzyme (ACE) is involved in the production of angio-
tensin II; thus, its inhibition will lower the levels of this
hormone.11 Consequently, there is a decrease in aldo-
sterone and an activation of bradykinin (a potent
vasodilator), which further reduces BP.
The ARBs will antagonize the effects of angiotensin II
by blocking its action at the receptor level. Renin blockers
will inhibit the production of angiotensin I, a precursor to
angiotensin II, once again affecting the RAS system.
ACEIs, ARBs, and renin inhibitors increase levels of
bradykinin in the system. Bradykinin will contribute to
the vasodilatory effects of these antihypertensive med-
ications, and this effect is mediated through stimulation
of PGE2 synthesis, as seen in animal studies.48 NSAIDs,
by virtue of inhibiting the PG synthesis, can interfere
with the vasodilatory effects of bradykinin and angio-
tensin II. This effect is more pronounced in individuals
with hypertension who have low renin levels.18
Vasodilators
Vasodilators are rarely used as primary medications to
control hypertension. The exact mechanism of vasodi-
lators is unknown, but it is believed, based on animal
experiments, to be mediated by the PG pathways49
through relaxation of smooth muscles in arterioles. The
relaxation of the smooth muscles decreases resistance in
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Volume 117, Number 6
the arterioles and hence reduces BP. On the other hand,
the vasodilators increase plasma renin concentration,
resulting in an increase in sodium and water retention.
There are very few data regarding their interaction with
NSAIDs.18 Their vasodilatory effect may be inhibited
through the inhibition of the RAS by NSAIDs.
Sympatholytic agents
Agents in this group modulate BP centrally by exerting
their agonistic action at the a2-adrenoreceptor, or
peripherally by blocking the a-adrenoreceptor or b-
adrenoreceptor. These are G-protein coupled receptors
that block calcium influx.
The centrally acting agents reduce the release of cat-
echolamines; consequently, there is a failure to activate
the sympathetic reflex arc pathway at the brain stem
vasomotor center, which is associated with aortic baro-
receptors involved in BP homeostasis. There is reduced
sympathetic flow to the peripheral cardiovascular sys-
tem, which decreases cardiac output. The sympatholytic
agents are rarely used in hypertension therapy because of
their systemic widespread undesirable effects. Never-
theless, clonidine is still prescribed for patients having
drug-resistant hypertension. These medications are not
directly affected by concomitant use of NSAIDs.18
The peripherally acting a1-adrenoreceptor antagonists
exert a vasodilatory effect on arterioles and venules,
which consequently reduces the peripheral vascular
resistance. The peripherally acting a1-adrenoreceptor
antagonist also reduces sodium reabsorption in the
kidneys, thus promoting excretion of fluids. Conse-
quently, the NSAIDs will affect this class of medication
by inhibiting PGE2 in the renal tubules, which promotes
sodium reabsorption and fluid retention.21,50
The b-blockers block the action of epinephrine and
norepinephrine at the b-adrenergic receptors. The antihy-
pertensive effects are primarily through stimulation of b1
receptors found in the myocardium and the kidney. At the
cardiovascular level, these agents lower cardiac output and
inhibit release of renin, which consequently affects the
RAS by lowering production of angiotensin and aldoste-
rone. NSAIDs inhibit renin release as well. With less renin
in the system, the effect of b1 selective blockers is blunt-
ed.18 Propranolol is a nonselective b-blocker, acting on b1
and b2 receptors. Propranolol has been found to stimulate
PGI2 synthesis, which in turn promotes vasodilation.51
NSAIDs block PGI2 synthesis, thus negating the effec-
tiveness of propranolol at the PGI2 level.34
Calcium channel blockers
Calcium channel blockers inhibit calcium influx in
smooth muscle cells, resulting in vasodilation of ar-
teries and reduced cardiac output. Morgan and Ander-
son (2003) performed a double-blind crossover study
REVIEW ARTICLE
Khatchadourian, Moreno-Hay and de Leeuw 701
comparing use of indomethacin in patients taking either
calcium channel blockers or ACEIs. They concluded
that indomethacin had less effect on calcium channel
blocking agents than on ACEIs.52 Similarly, in another
randomized controlled trial, Houston et al.53 found no
significant differences in BP when naproxen or
ibuprofen were added to the regimens of patients with
well-controlled hypertension taking verapamil.
Most major antihypertensives exert their effect,
completely or partially, through the PG-mediated
mechanisms, except for calcium channel blockers52 and
possibly b-blockers and a2-adrenoreceptor agonists.18
It is likely that NSAIDs’ interference with intrarenal
blood flow through PG inhibition is the main reason for
the BP-raising effect,34 thus antagonizing the effects of
antihypertensive drugs and consequently increasing
hypertension-related morbidity.14,18
A prospective clinical trial of 88 treated patients with
hypertension54 found that all antihypertensive medica-
tions except calcium channel blockers are affected by
NSAIDs’ vasoconstrictive effect, confirming findings in
several review articles.18,44,55 The trial found stronger
effects in hypertensive vs normotensive participants and
found that they were dose-dependent, similar to results
found in a review article35 and 2 meta-analyses of
clinical data.50,56
On the other hand, a recent cohort study compared the
effect of NSAIDs on different antihypertensive drugs,
including ACEIs, calcium channel blockers, b-blockers,
a-blockers, and diuretics. This study found that di-
uretics, ACEIs, and calcium channel blockers were
affected by NSAIDs, whereas b-blockers were not.57 A
review article published in 2006 ranked the effect of
NSAIDs on antihypertensive drugs in the following
order of severity of interaction: ACEIs/ARBs, diuretics,
b-blockers, and calcium antagonists or a-blockers.55
Sheridan et al.58 stated that nonpharmacologic con-
founding factors, such as sodium intake and exercise,
affect the BP readings and are hard to account for. They
concluded that the effect of NSAIDs on increasing BP
significantly is debatable. Moreover, other potential
confounding factors should be controlled in patients
with inadequately controlled hypertension.
CONCLUSION
Most studies have found that short-term use of NSAIDs
does not pose a major risk for hypertension or increase
in CVD. It is likely that NSAIDs’ interference with
RAS is the main reason for the BP-raising effect, and
the extent is variable. Patients with hypertension appear
to be more susceptible than normotensive participants
to the BP-increasing effect of NSAIDs. Given that the
elderly are more likely to use NSAIDs and that they
have a higher prevalence of hypertension than the
younger population, this group should be considered
ORAL MEDICINE
702 Khatchadourian, Moreno-Hay and de Leeuw
more susceptible to this effect as well. Of all the BP
medications, the calcium channel blockers and b-
blockers seem to be least affected by the concomitant
use of NSAIDs. Sympatholytic agents are also among
the least affected drugs; however, they are not often
used for BP control. Of all the NSAIDs, piroxicam,
naproxen, and indomethacin seem to have the highest
hypertensive effect, especially in patients with hyper-
tension. Celecoxib has a similar hypertensive effect as
nonselective NSAIDs in short-term studies but may
have an increased effect on hypertension when used
over longer periods.
A dentist must weigh the benefits and disadvantages of
using NSAIDs in patients taking antihypertensive drugs.
Conservative, short-term therapy should not be an issue
for most of these patients. Caution is also recommended
when prescribing NSAIDs in patients with a history of GI
disease, CVD, diabetes, or renal or hepatic impairment.
For those who may be at a greater risk, careful selection of
the class of NSAID and close monitoring are appropriate
measures, especially if long-term use is anticipated.
Other classes of analgesics may also be considered, such
as opioids and acetaminophen. As dentists, we belong to
the health care team responsible for the overall man-
agement of health issues in our patients.
We thank Ms Aline Shogher Markarian, BPharm, DESS, for
her comments and critical review of this publication.
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