How does NSAIDs cause hypertension?
Drug-induced hypertension associated with NSAIDs is due to the renal effects of these drugs. Specifically, NSAIDs cause dose-related increases in sodium and water retention. This effect is also seen with COX-2 selective agents, such as celecoxib.
What is the mechanism of action for NSAIDs?
The main mechanism of action of NSAIDs is the inhibition of the enzyme cyclooxygenase (COX). Cyclooxygenase is required to convert arachidonic acid into thromboxanes, prostaglandins, and prostacyclins. [9] The therapeutic effects of NSAIDs are attributed to the lack of these eicosanoids.
Can hypertensive patients take NSAIDs?
Given the current literature, it appears that NSAIDs increase blood pressure in patients with controlled-hypertension, but the quantity of this increase is variable. If possible, patients who have hypertension should avoid taking NSAIDs.
How do NSAIDs cause sodium retention?
NSAIDs promote sodium and water retention, and this has generally been explained by a reduction in prostaglandin-induced inhibition of both renal chloride reabsorption and the action of antidiuretic hormone. The same mechanism has been used to explain the reduction in effectiveness of antihypertensive drugs.
Are NSAIDs Vasoconstrictors?
NSAIDs, by inhibition of prostaglandins and bradykinin, produce vasoconstriction of the afferent renal arteriole and reduce the ability of the kidney to regulate (increase) glomerular blood flow.
What receptors do NSAIDs act on?
NSAIDs work by inhibiting the activity of cyclooxygenase enzymes (COX-1 or COX-2). In cells, these enzymes are involved in the synthesis of key biological mediators, namely prostaglandins, which are involved in inflammation, and thromboxanes, which are involved in blood clotting.
What is the mechanism of action of celecoxib?
The mechanism of action of celecoxib is due to selective inhibition of cyclooxygenase-2 (COX-2), which is responsible for prostaglandin synthesis, an integral part of the pain and inflammation pathway. [3] This pharmacologic activity gives celecoxib its analgesic, anti-inflammatory, and antipyretic effects.
Why are NSAIDs contraindicated in hypertension?
They are often used to relieve pain or reduce inflammation from conditions such as arthritis. However, NSAIDs can make your body retain fluid and decrease the function of your kidneys. This may cause your blood pressure to rise even higher, putting greater stress on your heart and kidneys.
Why is ibuprofen contraindicated in hypertension?
Ibuprofen and other NSAIDs may be associated with modest increases in blood pressure. NSAIDs may blunt the effects of common classes of antihypertensive medicine, including diuretics.
What are the pharmacodynamics of NSAIDs?
The therapeutic effects of NSAIDs are mediated chiefly through the inhibition of prostaglandin synthesis. Prostanoids are formed enzymatically through prostaglandin–endoperoxide synthases 1 and 2 (PGHS-1 and PGHS-2), which are also known as cyclooxygenases 1 and 2 (COX-1 and COX-2) .
How do NSAIDs inhibit prostaglandin synthesis?
NSAIDs generally work by blocking the production of prostaglandins (PGs) through the inhibition of two cyclooxygenase enzymes. PGs are key factors in many cellular processes, such as gastrointestinal cytoprotection, hemostasis and thrombosis, inflammation, renal hemodynamics, turnover of cartilage, and angiogenesis.