Detail of "21778-69-8"

Reference

Enkephalin degradation by enkephalinergic neuroblastoma cells

Enkephalin degradation by enkephalinergic neuroblastoma cells. Involvement of angiotensin-converting-enzyme. Palenker, J.; Lentzen, H.; Brandt, U. (Pharmakol. Inst., Freien Univ. Berlin, Berlin D-1000/33, Fed. Rep. Ger.).Several reagents with their cas registry numbers 58822-25-6 and 60-18-4 are used here. Naunyn-Schmiedeberg's Arch. Pharmacol., 325(3), 214-17 (English) 1984. CODEN: NSAPCC. ISSN: 0028-1298. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Degrdn. of tritiated [Leu5]enkephalin [58822-25-6] was studied in cultures of neuroblastoma cells (clone N1E-115). Incubation of cells in suspension revealed Tyr [60-18-4] as the main tritiated metabolite; however, Tyr-Gly-Gly [21778-69-8] and Tyr-Gly [673-08-5] were detectable as well. In a crude membrane prepn. of the neuroblastoma cells the level of Tyr is reduced to 13% and that of Tyr-Gly to 10% of the initial value, whereas Tyr-Gly-Gly is increased to about 5 times the initial value. Of the degraded enkephalin, 66% was accounted for by the formation of Tyr, 30% by the formation of Tyr-Gly-Gly, and 4% by the formation of Tyr-Gly. The prodn. of Tyr was inhibited by bestatin, an inhibitor of aminopeptidase [9031-94-1], and that of Tyr-Gly-Gly by captopril, an inhibitor of angiotensin-converting-enzyme [9015-82-1]. Evidently, neuroblastoma cells (N1E-115) degrade enkephalin by aminopeptidase and the membrane-bound angiotensin-converting-enzyme. .

Structure-activity evidence against opiate receptor involvement in Leu5-enkephalin-induced pulmonary vasoconstriction

Structure-activity evidence against opiate receptor involvement in Leu5-enkephalin-induced pulmonary vasoconstriction. Crooks, Peter A.; Bowdy, Bruce D.; Reinsel, Carol N.; Iwamoto, Edgar T.; Gillespie, Mark N. (Lexington, KY, USA). Biochem. Pharmacol., 33(24), 4095-8 (English) 1984. CODEN: BCPCA6. ISSN: 0006-2952. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Evidence was presented that indicates that leucine-enkephalin (I) [58822-25-6]-induced pulmonary vasoconstriction in the isolated rat heart-lung prepn. does not involve activation of conventional opiate receptors and does not require I metab. by lung peptidases. Methionine-enkephalin [58569-55-4] and D-Ala2,D-Leu5-enkephalin [63631-40-3] were inactive at doses twice that of I. The d opiate receptor antagonist diprenorphine had no effect on I-induced pulmonary vasoconstriction. The peptidase inhibitors bestatin and captopril augmented rather than inhibited the action of I, thus indicating that metab. or degrdn. of I is not responsible for its pressor action. Of the 4 fragments of I: Gly-Gly-Phe-Phe (II) [95599-35-2], Tyr-Gly-Gly [21778-69-8], Tyr-Gly [673-08-5], and Phe-Leu [3303-55-7], only II was active, and only at a rate 20% that of I. The nonopiate receptor involvement in the action I is reinforced in view of previous work that showed that I action is not blocked by naloxone, naltrexone, or mimicked by morphine.