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Reduction of myocardial injury by the EP3 receptor agonist TEI-3356. Role of protein kinase C and of K(ATP)-channels.
Eur J Pharmacol. 1999 Feb 12; 367(1):33-9.EJ

Abstract

The effects of the prostanoid EP3 receptor agonist TEI-3356 on either protein kinase C or ATP-sensitive (K(ATP)) K+ channels and on the infarct size caused by regional myocardial ischaemia and reperfusion in the rat were investigated. Male Wistar rats (n = 72) were subjected to 25 min occlusion of the left anterior descending coronary artery followed by 2 h of reperfusion. TEI-3356 (1 microg/kg/min i.v., n = 6) caused a significant reduction in infarct size from 60+/-3% (control, n = 8) to 38+/-3% of the area at risk. Pretreatment of rats with 5-hydroxydecanoate (5 mg/kg i.v., n = 6), a specific inhibitor of K(ATP)-channels, attenuated the cardioprotective effects of TEI-3356. The reduction in infarct size afforded by TEI-3356 was also abolished by the protein kinase C inhibitors staurosporine (1 microg/kg i.v., n = 6) and chelerythrine (0.7 mg/kg i.v., n = 5). Thus, TEI-3356 reduces myocardial infarct size in the rat by a mechanism(s) which involves the activation of protein kinase C and the opening of K(ATP)-channels.

Authors+Show Affiliations

The William Harvey Research Institute, St. Bartholomew's and The Royal London School of Medicine and Dentistry, UK.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10082262

Citation

Zacharowski, K, et al. "Reduction of Myocardial Injury By the EP3 Receptor Agonist TEI-3356. Role of Protein Kinase C and of K(ATP)-channels." European Journal of Pharmacology, vol. 367, no. 1, 1999, pp. 33-9.
Zacharowski K, Olbrich A, Thiemermann C. Reduction of myocardial injury by the EP3 receptor agonist TEI-3356. Role of protein kinase C and of K(ATP)-channels. Eur J Pharmacol. 1999;367(1):33-9.
Zacharowski, K., Olbrich, A., & Thiemermann, C. (1999). Reduction of myocardial injury by the EP3 receptor agonist TEI-3356. Role of protein kinase C and of K(ATP)-channels. European Journal of Pharmacology, 367(1), 33-9.
Zacharowski K, Olbrich A, Thiemermann C. Reduction of Myocardial Injury By the EP3 Receptor Agonist TEI-3356. Role of Protein Kinase C and of K(ATP)-channels. Eur J Pharmacol. 1999 Feb 12;367(1):33-9. PubMed PMID: 10082262.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reduction of myocardial injury by the EP3 receptor agonist TEI-3356. Role of protein kinase C and of K(ATP)-channels. AU - Zacharowski,K, AU - Olbrich,A, AU - Thiemermann,C, PY - 1999/3/19/pubmed PY - 1999/3/19/medline PY - 1999/3/19/entrez SP - 33 EP - 9 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 367 IS - 1 N2 - The effects of the prostanoid EP3 receptor agonist TEI-3356 on either protein kinase C or ATP-sensitive (K(ATP)) K+ channels and on the infarct size caused by regional myocardial ischaemia and reperfusion in the rat were investigated. Male Wistar rats (n = 72) were subjected to 25 min occlusion of the left anterior descending coronary artery followed by 2 h of reperfusion. TEI-3356 (1 microg/kg/min i.v., n = 6) caused a significant reduction in infarct size from 60+/-3% (control, n = 8) to 38+/-3% of the area at risk. Pretreatment of rats with 5-hydroxydecanoate (5 mg/kg i.v., n = 6), a specific inhibitor of K(ATP)-channels, attenuated the cardioprotective effects of TEI-3356. The reduction in infarct size afforded by TEI-3356 was also abolished by the protein kinase C inhibitors staurosporine (1 microg/kg i.v., n = 6) and chelerythrine (0.7 mg/kg i.v., n = 5). Thus, TEI-3356 reduces myocardial infarct size in the rat by a mechanism(s) which involves the activation of protein kinase C and the opening of K(ATP)-channels. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/10082262/Reduction_of_myocardial_injury_by_the_EP3_receptor_agonist_TEI_3356__Role_of_protein_kinase_C_and_of_K_ATP__channels_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(98)00963-7 DB - PRIME DP - Unbound Medicine ER -