NSAIDs and acetaminophen Effects on hypertension
INTRODUCTION — Patients being treated for hypertension may have increased activation of the renin-angiotensin and sympathetic nervous system. These vasoconstrictors increase the release of vasodilator prostaglandins from the kidney, which act locally to minimize the degree of renal ischemia.
When this compensatory response is inhibited by a nonsteroidal antiinflammatory drug (NSAID), the increase in renal and systemic vascular resistance can cause an elevation in blood pressure (BP). It can also cause acute renal failure in selected patients and worsening of heart failure.
These complications can generally be induced by any NSAID (including the relatively selective COX-2 inhibitors), but may be less likely to occur with sulindac or low-dose aspirin (see below) or with other types of analgesics such as acetaminophen .
The following discussion will emphasize the data on the nonselective NSAIDs that inhibit both COX-1 and COX-2. The data on the selective COX-2 inhibitors are presented in detail elsewhere.