کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5737399 | 1614711 | 2017 | 28 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Modulation of cardiac vagal tone by bradykinin acting on nucleus ambiguus
ترجمه فارسی عنوان
مدولاسیون تن وحشی قلب توسط برادیکینین بر روی هسته اومبیگوس
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کلمات کلیدی
HBSSIP3nAmb1,4,5-trisphosphate - 1،4،5-تری فسفاتAUC - AUCDiBAC4(3) - DiBAC4 (3)[Ca2+]i - [Ca2 +] ibradykinin - برادیکینینVagal tone - تن وگالCardiovascular regulation - تنظیم قلب و عروقCalcium signaling - سیگنالینگ کلسیمCytosolic Ca2+ concentration - غلظت Ca2 + سیتواستولیHank’s balanced salt solution - محلول نمک متعادل هانکarea under curve - منطقه تحت منحنیMicroinjection - میکروکنترلرnucleus ambiguus - هسته ابهامB1 receptor - گیرنده B1B2 receptor - گیرنده B2
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Bradykinin (BK), a component of the kallikrein-kininogen-kinin system exerts multiple effects via B1 and B2 receptor activation. In the cardiovascular system, bradykinin has cardioprotective and vasodilator properties. We investigated the effect of BK on cardiac-projecting neurons of nucleus ambiguus, a key site for the parasympathetic cardiac regulation. BK produced a dose-dependent increase in cytosolic Ca2+ concentration. Pretreatment with HOE140, a B2 receptor antagonist, but not with R715, a B1 receptor antagonist, abolished the response to BK. A selective B2 receptor agonist, but not a B1 receptor agonist, elicited an increase in cytosolic Ca2+ similarly to BK. Inhibition of N-type voltage-gated Ca2+ channels with Ï-conotoxin GVIA had no effect on the Ca2+ signal produced by BK, while pretreatment with Ï-conotoxin MVIIC, a blocker of P/Q-type of Ca2+ channels, significantly diminished the effect of BK. Pretreatment with xestospongin C and 2-aminoethoxydiphenyl borate, antagonists of inositol 1,4,5-trisphosphate receptors, abolished the response to BK. Inhibition of ryanodine receptors reduced the BK-induced Ca2+ increase, while disruption of lysosomal Ca2+ stores with bafilomycin A1 did not affect the response. BK produced a dose-dependent depolarization of nucleus ambiguus neurons, which was prevented by the B2 receptor antagonist. In vivo studies indicate that microinjection of BK into nucleus ambiguus elicited bradycardia in conscious rats via B2 receptors. In summary, in cardiac vagal neurons of nucleus ambiguus, BK activates B2 receptors promoting Ca2+ influx and Ca2+ release from endoplasmic reticulum, and membrane depolarization; these effects are translated in vivo by bradycardia.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 365, 4 December 2017, Pages 23-32
Journal: Neuroscience - Volume 365, 4 December 2017, Pages 23-32
نویسندگان
Eugen Brailoiu, Matthew McGuire, Shadaria A. Shuler, Elena Deliu, Jeffrey L. Barr, Mary E. Abood, G. Cristina Brailoiu,