Compounds > arg-(3-hyp-5-thi-7-tic-9-oic)-9-desarg-bradykinin

arg-(3-hyp-5-thi-7-tic-9-oic)-9-desarg-bradykinin and Reperfusion-Injury

arg-(3-hyp-5-thi-7-tic-9-oic)-9-desarg-bradykinin has been researched along with Reperfusion-Injury* in 1 studies

Other Studies

1 other study(ies) available for arg-(3-hyp-5-thi-7-tic-9-oic)-9-desarg-bradykinin and Reperfusion-Injury

Article	Year
Dual signaling via protein kinase C and phosphatidylinositol 3'-kinase/Akt contributes to bradykinin B2 receptor-induced cardioprotection in guinea pig hearts. Journal of molecular and cellular cardiology, 2001, Volume: 33, Issue:11 We investigated the role of protein kinase C (PKC) and phosphatidylinositol 3;-kinase (PI3-K) in the signaling mechanism of cardioprotection afforded by bradykinin (BK). Coronary-perfused guinea pig ventricular muscles were subjected to 20-min no-flow ischemia and 60-min reperfusion. Pretreatment for 5 min with BK (1 microm) significantly improved the recovery of developed tension measured after 60 min of reperfusion (86.8+/-2.6%v 34.8+/-4.1% in control). Prior treatment with B2 receptor antagonist HOE 140 completely abolished the protective effect of BK (37.0+/-7.6%). The protection was reduced by either PKC inhibitor chelerythrine (CH, 58.9+/-2.2%) or PI3-K inhibitor wortmannin (WM, 59.4+/-2.5%); however, the recovery of contractility was intermediate between the BK and control groups. Nevertheless, pretreatment with CH and WM together completely eliminated the protective effect of BK (38.9+/-4.2%). The mitochondrial ATP-sensitive K+ (mitoK(ATP)) channel blocker 5-hydroxydecanoate (5HD) significantly but partially inhibited the effect of BK (59.0+/-2.2%). Pretreatment with 5HD and CH together could not generate further inhibition (61.1+/-3.3%), while pretreatment with 5HD and WM together totally eliminated the protection (34.9+/-2.9%). We conclude that BK B2 receptors can precondition guinea pig hearts via the dual activation of PKC and PI3-K. The mitoK(ATP) channels act as downstream targets of PKC, whereas PI3-K is not associated with mitoK(ATP) channels. Topics: Alkaloids; Animals; Anti-Arrhythmia Agents; Benzophenanthridines; Blotting, Western; Bradykinin; Decanoic Acids; Enzyme Inhibitors; Guinea Pigs; Heart; Hydroxy Acids; Mitochondria; Myocardium; Phenanthridines; Phosphatidylinositol 3-Kinases; Phosphorylation; Protein Binding; Protein Kinase C; Protein Serine-Threonine Kinases; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-akt; Receptor, Bradykinin B2; Receptors, Bradykinin; Reperfusion; Reperfusion Injury; Signal Transduction; Tetrahydroisoquinolines; Time Factors	2001

Article

Year

Dual signaling via protein kinase C and phosphatidylinositol 3'-kinase/Akt contributes to bradykinin B2 receptor-induced cardioprotection in guinea pig hearts.

Journal of molecular and cellular cardiology, 2001, Volume: 33, Issue:11

We investigated the role of protein kinase C (PKC) and phosphatidylinositol 3;-kinase (PI3-K) in the signaling mechanism of cardioprotection afforded by bradykinin (BK). Coronary-perfused guinea pig ventricular muscles were subjected to 20-min no-flow ischemia and 60-min reperfusion. Pretreatment for 5 min with BK (1 microm) significantly improved the recovery of developed tension measured after 60 min of reperfusion (86.8+/-2.6%v 34.8+/-4.1% in control). Prior treatment with B2 receptor antagonist HOE 140 completely abolished the protective effect of BK (37.0+/-7.6%). The protection was reduced by either PKC inhibitor chelerythrine (CH, 58.9+/-2.2%) or PI3-K inhibitor wortmannin (WM, 59.4+/-2.5%); however, the recovery of contractility was intermediate between the BK and control groups. Nevertheless, pretreatment with CH and WM together completely eliminated the protective effect of BK (38.9+/-4.2%). The mitochondrial ATP-sensitive K+ (mitoK(ATP)) channel blocker 5-hydroxydecanoate (5HD) significantly but partially inhibited the effect of BK (59.0+/-2.2%). Pretreatment with 5HD and CH together could not generate further inhibition (61.1+/-3.3%), while pretreatment with 5HD and WM together totally eliminated the protection (34.9+/-2.9%). We conclude that BK B2 receptors can precondition guinea pig hearts via the dual activation of PKC and PI3-K. The mitoK(ATP) channels act as downstream targets of PKC, whereas PI3-K is not associated with mitoK(ATP) channels.

Topics: Alkaloids; Animals; Anti-Arrhythmia Agents; Benzophenanthridines; Blotting, Western; Bradykinin; Decanoic Acids; Enzyme Inhibitors; Guinea Pigs; Heart; Hydroxy Acids; Mitochondria; Myocardium; Phenanthridines; Phosphatidylinositol 3-Kinases; Phosphorylation; Protein Binding; Protein Kinase C; Protein Serine-Threonine Kinases; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-akt; Receptor, Bradykinin B2; Receptors, Bradykinin; Reperfusion; Reperfusion Injury; Signal Transduction; Tetrahydroisoquinolines; Time Factors

2001