While canonical transient receptor potential (TRPC) channels are ubiquitously present, the isoform distribution of the TRPCs and the native makeup of the TRPC heteromers are cell type and tissue specific. All the seven members of the TRPC channels, designated as TRPC1-TRPC7 (TRPC2 is absent in human), are classified as Ca2+-permeable, non-selective cation channels. Physiologically, the channel activation is triggered by activation of phosphalipase C pathway following activation of G-proteincoupled receptors or receptor tyrosine kinases. TRPCs have been known to participate in a wide range of cell function, including contraction and proliferation of vascular smooth muscle cells. Recently, growing evidence has emerged that specific isoforms of TRPCs exist in renal microvasculature and contribute to hormone-induced renal responses, such as renal blood flow and glomerular filtration. This review article summarized the recent progress in this scenario, emphasizing the TRPC channels expressed inside renal microvasculature as well as in glomerular cells (outside microvasculature) that regulate renal microcirculation. The possible mechanism(s) underlying the TRPC-mediated responses, i.e. store-operated, receptor-operated or Na+-Ca2+ exchange mechanism, are discussed. In addition, we included recent findings from other's and our groups in this article to demonstrate an association of TRPC channels, particularly TRPC6, in microcirculatory system with kidney diseases. The aim of the review is to advance our understanding of renal physiology and pathophysiology at the cellular and molecular levels.
|Title of host publication||Microcirculation|
|Subtitle of host publication||Function, Malfunction and Measurement|
|Publisher||Nova Science Publishers, Inc.|
|Number of pages||14|
|State||Published - 1 Apr 2009|