کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9921537 | 1559226 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
K+-induced vasodilation in the rat kidney is dependent on the endothelium and activation of K+ channels
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موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
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چکیده انگلیسی
Increased extracellular K+ is reported to cause endothelium-independent vasodilation and K+ has been proposed as an endothelium-derived hyperpolarizing factor. However, the endothelium is endowed with K+ channels that may also be responsive to increased K+. We examined the vasodilator effect of bolus administration of 20, 40 and 60 μmol KCl in the rat isolated kidney in which perfusion pressure was elevated with phenylephrine. KCl produced dose-dependent vasodilator responses that were virtually abolished by removal of the endothelium which also abolished the vasodilator effect of bradykinin without affecting that to nitroprusside. The vasodilator effect of KCl was unaffected by inhibition of cyclooxygenase, nitric oxide synthase or cytochrome P450 but reduced by inhibition of K+ channels with tetraethylammonium (TEA). Barium chloride reduced the vasodilator effects of KCl but charybdotoxin/apamin was without effect. These results indicate that KCl results in endothelium-dependent vasodilation that is independent of nitric oxide (NO), prostaglandins and cytochrome P450 but dependent on activation of endothelial K+ channels.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Pharmacology - Volume 508, Issues 1â3, 31 January 2005, Pages 193-199
Journal: European Journal of Pharmacology - Volume 508, Issues 1â3, 31 January 2005, Pages 193-199
نویسندگان
John Quilley, Yue Qiu,