Do COX-2 inhibitors affect kidneys?
Like other NSAIDs, COX-2 inhibitors can cause salt and water retention, leading to edema and worsening hypertension. They can also cause acute declines in renal function and glomerular filtration rate.
What are COX-2 inhibitors used for?
COX-2 inhibitors are used for treating conditions that cause inflammation, mild to moderate pain, and fever.
How do NSAIDs affect ADH?
Studies in humans and animals have shown that the effect of ADH is potentiated by NSAIDs . Prostaglandins are present in the kidney and inhibit the water reabsorption effect of ADH. NSAIDs decrease prostaglandin formation and therefore the effect of ADH is potentiated.
How do NSAIDs affect sodium?
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.
Do Cox-2 inhibitors raise BP?
Background: Both COX-2 selective inhibitors (coxibs) and nonselective (ns)-NSAIDs elevate blood pressure (BP) and this may contribute to excess cardiovascular (CV) events.
What does Cox do in the kidney?
In the kidney, COX-2 is constitutively expressed and is highly regulated in response to alterations in intravascular volume. COX-2 metabolites have been implicated in the mediation of renin release, regulation of sodium excretion, and maintenance of renal blood flow.
What effect does a cyclooxygenase inhibitor have?
COX-2 inhibitors are NSAIDs that selectively block the COX-2 enzyme and not the COX-1 enzyme. Blocking this enzyme impedes the production of prostaglandins by the COX-2 which is more often the cause the pain and swelling of inflammation and other painful conditions.
Why do NSAIDs ibuprofen cause hyperkalemia?
The hypothesized mechanism for hyperkalemia associated with NSAIDs is related to the inhibition of prostacyclin. In contrast to COX-1, COX-2 mediates prostacyclin synthesis, which increases potassium secretion at the distal tubule.
How do NSAIDs reduce sodium excretion?
These results suggest that NSAID may inhibit the intrarenal role of prostaglandins and decrease sodium and water excretion in urine with resulting increased body fluid volume. Tolerance to these actions of NSAID developed after repeated administration.
Why does NSAIDs cause hyperkalemia?
Do Cox 2 inhibitors raise blood pressure more than nonselective NSAIDs and placebo An updated meta analysis?
These results were mainly driven by rofecoxib, with a RR of 1.87 (1.63-2.14, P = 0.08) versus placebo, and etoricoxib, with a RR of 1.52 (1.39-1.66, P = 0.01) versus ns-NSAID. Conclusion: On the basis of this updated meta-analysis, coxibs appear to produce greater hypertension than either ns-NSAIDs or placebo.
What is the role of COX-2 inhibition in postobstructive kidney disease?
In the postobstructive kidney, COX-2 inhibition attenuates the downregulation of AQP2 and reduces polyuria acutely after the release of obstruction , .
What is the role of cyclooxygenase-2 inhibitors in the treatment of ureteral obstruction?
Cheng X., Zhang H., Lee H.L., Park J.M. Cyclooxygenase-2 inhibitor preserves medullary aquaporin-2 expression and prevents polyuria after ureteral obstruction. J Urol. 2004;172:2387–2390. [PubMed] [Google Scholar] 61.
Is prostaglandin E2 an important lipid mediator in kidney injury?
Keywords: Acute kidney injury, Cyclooxygenase, Obstructive nephropathy, Prostaglandin E2, Water balance Introduction Prostaglandins (PGs) are important lipid mediators of numerous physiological and pathophysiological processes in the kidney.
What is cyclooxygenase (COX)?
Abstract The cyclooxygenase (COX) enzyme system is the major pathway catalyzing the conversion of arachidonic acid into prostaglandins (PGs).