Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.5 (cathepsin D)
 4,130 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandin F2alpha concentrations were determined in hepatic portal venous plasma of dogs during splanchnic artery occlusion (SAO) shock and in nonshock control dogs. Dogs subjected to SAO shock exhibited a dramatic decrease in mean arterial blood pressure and significant increases in portal venous PGF2alpha and amino-nitrogen concentrations, as well as in cathepsin D and MDF activities. Dogs treated with indomethacin prior to SAO shock did not exhibit a significant increase in portal venous PGF2alpha. Indomethacin had no effect on the increase of plasma amino-nitrogen and only slightly reduced portal venous cathepsin D activity during SAO shock. Nevertheless, indomethacin significantly attenuated the severity of the postrelease hypotension observed in SAO shock and diminished the plasma accumulation of MDF. These studies indicate that prostaglandins are released from the splanchnic region during SAO shock and that this release can be prevented by pretreatment with indomethacin. The role of endogenously released prostaglandins in SAO shock is not clear, but the magnitude of the increase warrants further study.
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PMID:Release of prostaglandin F2alpha during splanchnic artery occlusion shock. 126 70

Indomethacin and naproxen were examined regarding their effects on glycosaminoglycan metabolism in normal albino rats. The biosynthesis of sulphated glycosaminoglycans as evaluated by the uptake of [35S-]sulphate and the content of glycosaminoglycans were measured in specimens of skin, liver and kidney. The results indicated that the biosynthesis of sulphated glycosaminoglycans was significantly inhibited by both these drugs, thus reflecting their anti-inflammatory properties. The catabolism of glycosaminoglycans was followed by estimating the activities of lysosomal glycohydrolases, viz., beta-glucuronidase, beta-N-acetyl glucosaminidase and cathepsin D in liver, kidney and spleen and urinary excretion of hexosamine and uronic acid. The results, considered collectively, indicated that both indomethacin and naproxen depressed the metabolism of glycosaminoglycans.
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PMID:Effect of indomethacin and naproxen on the metabolism of glycosaminoglycans. 717 58