کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10836124 | 1066405 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Bradykinin B2 type receptor activation regulates fluid and electrolyte transport in the rabbit kidney
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کلمات کلیدی
EGTAGi-proteinPGE2PIP2SSPSNKAVPCCD[Ca2+]i - [Ca2 +] iarginine-vasopressin - آرژنین واسپرسینstaurosporine - استوسوسورپینbradykinin - برادیکینینDiuresis - دیورزpertussis toxin - سموم سورافنیintracellular calcium ion concentration - غلظت یون کلسیم داخل سلولیphosphatidylinositol bisphosphate - فسفاتیدیلینوزیتول بیسفسفاتFluorescence ratio - نسبت فلورسانسHydraulic conductivity - هدایت هیدرولیکیProstaglandin E2 - پروستاگلاندین E2cortical collecting duct - کانال جمع آوری کورتنیcalcium ionophore - یونوفور کلسیم
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Bradykinin is an important autacoid produced in the kidney, regulating both renal function and blood pressure. In vivo studies in anesthetized rabbits, revealed that BK induced diuresis (UV), natriuresis (UNaV) and was not associated with renal hemodynamic changes. These diuretic and natriuretic effects were blocked by the BK-B2 antagonist HOE-140. BK also inhibits vasopressin (AVP)-stimulated water flow (Lp) in microperfused rabbit cortical collecting ducts (rCCD), in a concentration-dependent fashion, consistent with its in vivo diuretic effects. BK-B1 antagonist Leu8-des-Arg9-BK did not alter the effect of BK on Lp, but HOE-140 completely blocked the inhibitory effects of BK on Lp. While BK did not increase [Ca2+]i in fura-2 loaded freshly microdissected rCCD, BK increased [Ca2+]i in immortalized cultured rCCD cells demonstrating different signaling mechanisms are activated by BK in microdissected versus cultured rCCD. In microperfused rCCD, neither the protein kinase C inhibitor staurosporine nor the phospholipase C (PLC) inhibitor U-73,122 attenuated the BK response arguing against activation of PLC/PKC by BK in rCCD. We conclude: (1) BK induces UV and UNaV by a BK-B2 receptor; (2) BK inhibits AVP-stimulated Lp by a BK-B2 receptor suggesting that its effects on Lp are not via a PLC/PKC; (3) finally, BK raises [Ca2+]i in rCCD cells by a BK-B2 receptor mechanism.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Peptides - Volume 26, Issue 8, August 2005, Pages 1308-1316
Journal: Peptides - Volume 26, Issue 8, August 2005, Pages 1308-1316
نویسندگان
Richard L. Hébert, Domenico Regoli, Huaqi Xiong, Matthew D. Breyer, Gérard E. Plante,