کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2197299 | 1098877 | 2009 | 9 صفحه PDF | دانلود رایگان |
Angiotensin-II (Ang-II) exerts many of its vascular effects, including the pathophysiological changes associated with type 2 diabetes, through changes in intracellular calcium concentration [Ca2+]i. We sought to clarify the mechanism responsible for Ang-II-induced Ca2+ influx in cultured aortic VSMC using the Goto-Kakizaki (GK) rat model of type 2 diabetes. Ang-II-induced Ca2+ influx was blocked by neither VDCC nor c-src inhibition but was sensitive to inositol 1,4,5-trisphosphate receptor inhibition, lanthanide and the diacylglycerol analogue, oleoyl-2-acetyl-sn-glycerol. Since transient receptor potential canonical (TRPC)-3 gene expression was undetectable in both WKY and GK VSMCs and TRPC6 gene and protein expression were significantly down-regulated in GK, we believe the 1/4/5 subgroup of TRPC proteins plays a significant role. Furthermore, in GK VSMC the elevated calcium influx observed was not attributable to increased TRPC expression, but rather an alteration of TRPC activity.
Journal: Molecular and Cellular Endocrinology - Volume 302, Issue 1, 10 April 2009, Pages 49–57