کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2195774 1550862 2015 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Maternal hyperthyroidism increases the susceptibility of rat adult offspring to cardiovascular disorders
ترجمه فارسی عنوان
پرکاری تیروئید مادرانه حساسیت فرزندان بالاتری از موش به اختلالات قلب و عروق را افزایش می دهد
کلمات کلیدی
هیپرتیروئیدیسم حاملگی، سیستم قلبی رنین و آنژیوتانسین، برنامه ریزی جنینی
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
چکیده انگلیسی


• Maternal hyperthyroidism alters cardiac Renin Angiotensin System in adult offspring.
• Higher thyroid hormone levels in utero predisposes the offspring to cardiac disorders.
• Offspring from hyperthyroid dams presents a worse recovery after ischemic insult.
• Maternal hyperthyroidism is related to offspring's hypertension in later life.

Suboptimal intrauterine conditions as changed hormone levels during critical periods of the development are considered an insult and implicate in physiological adaptations which may result in pathological outcomes in later life. This study evaluated the effect of maternal hyperthyroidism (hyper) on cardiac function in adult offspring and the possible involvement of cardiac Renin-Angiotensin System (RAS) in this process. Wistar dams received orally thyroxin (12 mg/L) from gestational day 9 (GD9) until GD18. Adult offspring at postnatal day 90 (PND90) from hyper dams presented increased SBP evaluated by plethysmography and worse recovery after ischemia-reperfusion (I/R), as evidenced by decreased LVDP, +dP/dT and –dP/dT at 25 min of reperfusion and by increased infarct size. Increased cardiac Angiotensin I/II levels and AT1R in hyper offspring were verified. Herein, we provide evidences that maternal hyperthyroidism leads to altered expression of RAS components in adult offspring, which may be correlated with worse recovery of the cardiac performance after ischemic insults and hypertension.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 416, 15 November 2015, Pages 1–8
نویسندگان
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