title: Effects of nonsteroidal anti-inflammatory drug therapy on blood pressure and peripheral edema.
abstract: Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used drugs with potential effects on systemic blood pressure. NSAIDs act by inhibiting synthesis of prostaglandins (PGs) from arachidonic acid via cyclooxygenase (COX)-1 and COX-2, the 2 isoforms of COX. NSAIDs may affect blood pressure via the renin-angiotensin pathway, alterations in sodium and water retention in the kidneys, inhibition of vasodilating PGs, and production of various vasoconstricting factors, including endothelin-1 and P450-mediated metabolites of arachidonic acid. In 2 meta-analyses, it was found that NSAIDs have small but significant effects on blood pressure, most notably in hypertensive patients on antihypertensive medication. NSAIDs cause small (<5 mm Hg) elevations in systolic blood pressure, and little or no change in diastolic blood pressure. The incidence rates of hypertension and peripheral edema were low, ranging from <1% to >9% of patients. The incidence and levels of hypertension associated with COX-2 inhibitors are within the range of those observed with nonspecific NSAIDs. Apparent differences between the COX-2 inhibitors celecoxib and rofecoxib may be functions of differences in study population susceptibilities to NSAID-mediated hypertensive effects. Patients at risk for hypertension should be monitored for changes in blood pressure during NSAID treatment.
authors.affiliation: Department of Medicine, New York Medical College, Valhalla, New York 10595, USA. JOANNE_PRYOR@NYMC.EDU
authors.forename: William H
authors.initials: WH
authors.lastname: Frishman
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D001794:Blood Pressure / Q000187:drug effects*; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004341:Drug Evaluation / Q000379:methods; D004487:Edema / Q000139:chemically induced* / Q000453:epidemiology / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000139:chemically induced* / Q000453:epidemiology; D015994:Incidence; D007527:Isoenzymes / Q000037:antagonists & inhibitors; D008565:Membrane Proteins; D008875:Middle Aged; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases; D014882:Water-Electrolyte Balance / Q000187:drug effects
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D011448:Prostaglandin Antagonists; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases