Search results
Results from the WOW.Com Content Network
NSAIDs cause decreased ability to form blood clots, which can increase the risk of bleeding when combined with other drugs that also decrease blood clotting, such as warfarin. [113] NSAIDs may aggravate hypertension (high blood pressure) and thereby antagonize the effect of antihypertensives, [113] such as ACE inhibitors. [114]
Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a class of medication used primarily for the treatment of high blood pressure and heart failure. [1] [2] This class of medicine works by causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart.
As with other NSAIDs, potential side effects include gastrointestinal bleeding. [10] Long-term use has been associated with kidney failure, and rarely liver failure, and it can exacerbate the condition of patients with heart failure. [8] At low doses, it does not appear to increase the risk of heart attack; however, at higher doses it may. [10]
Aspirin and other NSAIDs can cause abnormally high blood levels of potassium by inducing a hyporeninemic hypoaldosteronism state via inhibition of prostaglandin synthesis; however, these agents do not typically cause hyperkalemia by themselves in the setting of normal renal function and euvolemic state. [225]
NSAIDs, naproxen and aspirin Blood thinners and anticoagulants, like warfarin, due to risk of abnormal bleeding Triptans and medications used to treat migraines like sumatriptan
Certain underlying health conditions can increase the risk of gout as well: Kidney disease. Obesity. Diabetes. High blood pressure. Heart disease. Taking certain types of medications can ...
Aldosterone binds to aldosterone receptors (mineralocorticoid receptors) increasing sodium reabsorption in an effort to increase blood pressure and improve fluid status in the body. When excessive sodium reabsorption occurs, there is an increasing loss of K + in the urine and can lead to clinically significant decreases, termed hypokalemia .
Nonsteroidal anti-inflammatory drugs (NSAIDs) alleviate pain by counteracting the cyclooxygenase (COX) enzyme. [1] On its own, COX enzyme synthesizes prostaglandins, creating inflammation. In whole, the NSAIDs prevent the prostaglandins from ever being synthesized, reducing or eliminating the inflammation and resulting pain. [citation needed]