title: [Role of B1 receptors in the endothelial protective effect of ischaemic preconditioning].
abstract: The aim of this study was to assess whether the cardioprotective effect of ischaemic preconditioning (IPC) on endothelial function in resistance coronary arteries of the rat involves activation of kinin receptors. Isolated rat hearts perfused under constant flow conditions were exposed to 30 min of partial ischaemia (flow rate 1 mL/min) followed by 20 min of reperfusion. Preconditioning was performed with 5 min zero-flow ischaemia and 10 min reperfusion before the 30-min ischaemia. After the 20-min reperfusion period, coronaries were precontracted with U-46619 0.1 microM, and the coronary response to the endothelium-dependent vasodilator, serotonin (5-HT, 10 microM), was compared to that of the endothelium-independent vasodilator, sodium nitroprusside (SNP, 3 microM). Kinin B1 and B2 receptors were blocked with perfusion of either [Lys0, Leu8, des-Arg0]-Bradykinin 30nM (LLDBK) or Hoe 140 10 nM (Hoe) respectively, started 15 min before IPC or a corresponding sham period and stopped just before the 20-min reperfusion period. In untreated hearts, ischemia diminished selectively 5-HT-induced vasodilatation, compared to sham hearts (without ischaemia). The vasodilatation by SNP was unaffected after ischaemia and reperfusion. Preconditioning in untreated hearts preserved the vasodilatation produced by 5-HT. Treatment of hearts with either Hoe or LLDBK had no effect on the vasodilatation produced by both 5-HT and SNP in sham hearts. Pre-treatment with Hoe did not block the protective effect of IPC on the 5-HT vasodilatation. LLDBK halved the protective effect of IPC on endothelium-dependent vasodilatation. In addition, the protective effect of BK on the endothelial function in the isolated rat heart was blocked by LLDBK. These results suggest that IPC and exogenous kinin perfusions afford protection to endothelial function in resistance coronary arteries of the rat partially by activation of B1 kinin receptors. B2 receptors do not play any role in that protection.
authors.affiliation: Facultésde pharmacie, Université de Montréal, Québec, Canada.
authors.forename: J F
authors.initials: JF
authors.lastname: Bouchard
authors.forename: J
authors.initials: J
authors.lastname: Chouinard
authors.forename: D
authors.initials: D
authors.lastname: Lamontagne
mesh_terms: D000818:Animals; D004730:Endothelium, Vascular / Q000502:physiology*; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018002:Receptors, Bradykinin / Q000502:physiology*; D012701:Serotonin / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D018002:Receptors, Bradykinin; D014665:Vasodilator Agents; D009599:Nitroprusside; D012701:Serotonin