نقش کانال‌های پتاسیمی در پاسخ انقباضی به یوروتنسین-2 در اختلال عملکردی القا شده به وسیله کلرید جیوه در اندوتلیوم آئورت موش صحرایی

نوع مقاله : مقاله کامل

نویسندگان

چکیده

یوروتنسین-2 (U-II)، قوی‌ترین ترکیب قابض عروقی که اخیرا به عنوان کاندیدی جدید در اختلالات قلبی عروقی مطرح شده است، ممکن است که اثر خود بر عروق را از طریق کانال‌های پتاسیمی که به وفور در اندوتلیوم و سلول‌های عضله صاف عروق (VSMCs) یافت می‌شوند، اعمال کند. مطالعه حاضر با هدف بررسی نقش کانال‌های پتاسیمی در پاسخ‌های عروقی به U-II، در اختلال عملکردی القا شده با جیوه در اندوتلیوم آئورت موش صحرایی و همچنین بافت سالم آئورت موش صحرایی انجام شده است. بدین منظور حلقه‌های آئورت با مسدود کنندگان پتاسیم شامل کاریبدوتوکسین (chtx)، تترا اتیل آمونیوم، کلرید باریم، گلی بن کلامید، آمینوپریدین-4 (4-AP) و کلوتریمازول انکوبه شده و سپس واکنش‌های عروقی به افزایش غلظت U-II انسانی در هر گروه در حضور و عدم حضور کلرید جیوه (HgCl2) ارزیابی شدند. کارآیی U-II در گروه‌های تیمار شده با chtx، تترا اتیل آمونیوم و کلرید باریم به طور معنی‌داری افزایش یافت در حالی که در گروه‌های تیمار شده با          گلی بن کلامید و کلوتریمازول به طور معنی‌داری در مقایسه با گروه شاهد کاهش یافت. در حضور جیوه، در همه گروه‌ها به جز گروه تیمار شده با کلوتریمازول، کارآیی U-II به طور معنی‌داری تغییر کرد. بر اساس یافته‌های این مطالعه، کانال‌های پتاسیمی پاسخ انقباضی عروق به U-II را در آئورت موش صحرایی کنترل می‌کنند و علاوه بر این تیمار با جیوه سبب افزایش کارآیی U-II و مدولاسیون سیگنالینگ پتاسیم می‌شود. 

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