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Hypertension. 2004;44:123-124
Published online before print June 28, 2004, doi: 10.1161/01.HYP.0000136129.18326.26
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(Hypertension. 2004;44:123.)
© 2004 American Heart Association, Inc.


Editorial Commentaries

Hypertension Associated With Therapies to Treat Arthritis and Pain

William B. White

From the Division of Hypertension and Clinical Pharmacology, Center for Cardiology and Cardiovascular Biology, University of Connecticut School of Medicine, Farmington.

Correspondence to William B. White, MD, Professor and Chief, Division of Hypertension and Clinical Pharmacology, Center for Cardiology and Cardiovascular Biology, University of Connecticut School of Medicine, 263 Farmington Ave, Farmington, CT 06030-3940. E-mail wwhite@nso1.uchc.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Cyclooxygenase-2 (COX-2) inhibitors have become a widely used class of agents for the treatment of arthritis and pain because of their improved gastrointestinal safety and tolerability profile compared with the nonselective NSAIDs.1,2 During the past 4 years, the effects of these agents on destabilization of blood pressure (BP) has become a concern that has led to substantial research and controversy. COX inhibition is associated with antinatriuretic and vasoconstrictor effects mediated through the inhibition of the actions of prostaglandin E2 and prostacylin.3–5 The first 2 studies that evaluated the effects of NSAIDs on BP6,7 demonstrated that mean arterial pressure could rise by as much as 5 to 6 mm Hg in a population of patients with hypertension. The greatest effects of NSAIDs on BP control were observed in patients on monotherapeutic regimens of ß-adrenergic blocking drugs, diuretics, or angiotensin-converting enzyme (ACE) inhibitors.6

Recent clinical trials suggest that patients treated with ß-blockers and ACE inhibitors are particularly susceptible to destabilization of BP control by some COX-2 inhibitors compared with patients controlled with a calcium antagonist.8 For example, in patients on an ACE inhibitor monotherapy regimen, rofecoxib (25 mg daily) increased the systolic BP by 5 mm Hg, whereas in patients on a calcium antagonist alone, there was no increase in systolic BP. However, not all COX-2 inhibitors have the same effect on BP. In a drug interaction trial involving 178 patients with hypertension, 24-hour ambulatory BP monitoring showed that celecoxib (200 mg twice daily) had a modest and nonsignificant increase in systolic . . . [Full Text of this Article]




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