Effect of the selective cox 2 inhibitor, rofecoxib versus the non selective cox inhibitor, indomethacin on renal hemodynamics and tubular excretion

Nonsteroidal anti-inflammatory drugs [NSAIDs] are among the most widely prescribed medications worldwide. The mechanism through which NSAIDs provide analgesia and suppress inflammation is the inhibition of the enzyme cyclooxygenase [COX] with subsequent suppression of the prostanoids synthesis. The suppression of prostanoids synthesis can also produce gastric and renal toxicity, as we!l as impair normal platelet function. Two distinct but related enzymes, cyclo-oxygenase-1 [COX-1] and cyclooxygenase-2 [COX-2] mediate prostanoids synthesis and contribute to the inflammatory process. However, it is generally assumed that NSAIDs anti-inflammatory and analgesic activity is mediated via COX-2 inhibition while Inhibition of COX-1 is thought to be responsible for the gastric toxicity and bleeding complications. It is unclear whether NSAID-induced renal toxicity is attributable to inhibition of COX-1 or COX-2. The present study was designed to compare the effect of chronic administration of selective COX-2 inhibitor, rofecoxib with that of the non selective COX inhibitor, in-domethacin on renal hemodynamics and tubular excretion. Thus, changes in mean arterial pressure [MAP], renal blood flow [RBF], glomerular filtration rate [GFR], urine volume and urinary Na 4 and K excretion ratio, hematocrite value, serum Na +.K +,urea and crearinine concentrations were all detected after IM injection of rofecoxib [1 umol/kg], indomethacin [3 umol/kg] or the vehicle for three weeks. Results from the present study showed that three weeks treatment with both indomethacin and rofecoxib induced a decrease in urine volume and Na + and K + excretion. Indomethacin but not rofecoxib reduced RBF and GFR. No significant change was observed in MAP, hematocrite value or serum Na + serum. Serum K + urea and creatinine levels were all elevated suggesting impairment in the renal functions. It seems likely that COX-2 inhibition causes acute salt and water retention, whereas the decline in RBF and GFR is caused by the blockade of COX-1. COX-2 inhibitors should be used with caution since they are, like traditional NSAIDs, can induce renal function impairment

Effect of acupuncture on blood pressure: role of opioid peptides

The effect of electroacupuncture on experimentally norepinephrine induced hypertension was studied on albino rats. In normotensive rats no significant change was observed in blood pressure with acupuncture insertion. The effect on experimentally induced hypertensive rats was contrary. As while insertion of needle at St.36 point resulted in a significant decrease in blood pressure, needle inserted at Go. 26 point resulted in a significant increase in blood pressure. Naloxone administration before acupuncture failed to inhibit its effects on blood pressure, indicating that acupuncture mediates its effects via opioid receptors other than mu receptors