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N-oleoyldopamine, a novel endogenous capsaicin-like lipid, protects the heart against ischemia-reperfusion injury via activation of TRPV1 Zhong B; Wang DHAm J Physiol Heart Circ Physiol 2008[Aug]; 295 (2): H728-35N-oleoyldopamine (OLDA), a bioactive lipid originally found in the mammalian brain, is an endovanilloid that selectively activates the transient receptor potential vanilloid type 1 (TRPV1) channel. This study tests the hypothesis that OLDA protects the heart against ischemia and reperfusion (I/R) injury via activation of the TRPV1 in wild-type (WT) but not in gene-targeted TRPV1-null mutant (TRPV1(-/-)) mice. Hearts of WT or TRPV1(-/-) mice were Langendorffly perfused with OLDA (2 x 10(-9) M) in the presence or absence of CGRP8-37 (1 x 10(-6) M), a selective calcitonin gene-related peptide (CGRP) receptor antagonist; RP-67580 (1 x 10(-6) M), a selective neurokinin-1 receptor antagonist; chelerythrine (5 x 10(-6) M), a selective protein kinase C (PKC) antagonist; or tetrabutylammonium (TBA, 5 x 10(-4) M), a nonselective K(+) channel antagonist, followed by 35 min of global ischemia and 40 min of reperfusion (I/R). Left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), coronary flow (CF), and left ventricular peak positive dP/dt (+dP/dt) were evaluated after I/R. OLDA improved recovery of cardiac function after I/R in WT but not TRPV1(-/-) hearts by increasing LVDP, CF, and +dP/dt and by decreasing LVEDP. CGRP8-37, RP-67580, chelerythrine, or TBA abolished the protective effect of OLDA in WT hearts. Radioimmunoassay showed that the release of substance P (SP) and CGRP after OLDA treatment was higher in WT than in TRPV1(-/-) hearts, which was blocked by chelerythrine or TBA. Thus OLDA exerts a cardiac protective effect during I/R injury in WT hearts via CGRP and SP release, which is abolished by PKC or K(+) channel antagonists. The protective effect of OLDA is void in TRPV1(-/-) hearts, supporting the notion that TRPV1 mediates OLDA-induced protection against cardiac I/R injury.|Animals[MESH]|Benzophenanthridines/pharmacology[MESH]|Calcitonin Gene-Related Peptide Receptor Antagonists[MESH]|Calcitonin Gene-Related Peptide/metabolism/pharmacology[MESH]|Coronary Circulation[MESH]|Dopamine/*analogs & derivatives/metabolism[MESH]|Isoindoles/pharmacology[MESH]|Male[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Mice, Knockout[MESH]|Myocardial Ischemia/complications/*metabolism/physiopathology[MESH]|Myocardial Reperfusion Injury/etiology/metabolism/physiopathology/*prevention & control[MESH]|Myocardium/*metabolism[MESH]|Neurokinin-1 Receptor Antagonists[MESH]|Peptide Fragments/pharmacology[MESH]|Potassium Channel Blockers/pharmacology[MESH]|Potassium Channels/metabolism[MESH]|Protein Kinase C/antagonists & inhibitors/metabolism[MESH]|Protein Kinase Inhibitors/pharmacology[MESH]|Quaternary Ammonium Compounds/pharmacology[MESH]|Radioimmunoassay[MESH]|Receptors, Calcitonin Gene-Related Peptide/metabolism[MESH]|Receptors, Neurokinin-1/metabolism[MESH]|Substance P/metabolism[MESH]|TRPV Cation Channels/deficiency/genetics/*metabolism[MESH]|Ventricular Function, Left[MESH]|Ventricular Pressure[MESH] |
