Study for expression and function of receptor operated TRPC channel in rat pulmonary small artery

BQ-123和BQ-788联合应用可部分抑制ET-1引起的肺动脉收缩和细胞内Ca^2+浓度（[Ca^2+] i）的升高。而BQ-123预处理可阻断ET-1引起的肾动脉收缩和[Ca^<2+>] i升高。SNP、SNAP和forskolin均能降低ET-1引起的肺动脉和肾动脉收缩和[Ca^<2+>]_i升高。但对肾动脉的影响较强。维拉帕米仅部分抑制ET-1引起的肾动脉[Ca^<2+>] i升高，而使肾动脉[Ca^<2+>] i几乎降低一半。尼卡地平可抑制ET-1引起的正常生理盐水（PSS）中[Ca^<2 +>] i的升高，但不抑制再加CaCl_2引起的[Ca^<2+] i的升高。环匹阿尼酸和毒胡萝卜素预孵育可抑制ET-1诱导的[Ca^<2+]_i升高，也可减弱ET-1诱导的[Ca^<2+]_i升高。磷脂酶C（PLC）抑制剂U-73122可显著降低ET-1诱导的无钙PSS [Ca^<2 +>]_i升高和随后的CaCl_2作用。2 APB和xestopongin C处理几乎完全抑制了[Ca^<2+>]_i的诱导增加。RT-PCR检测结果表明，TRPC 1、TRPC 4、TRPC 5、TRPC 6和LTRPC 7在组织中均有表达。这些结果表明，在大鼠肺小动脉对ET-1的反应中，存在受PLC下游控制的受体操纵的Ca^2+内流。

In pulmonary artery, combination treatment of BQ-123 and BQ-788 partially inhibited ET-1-induced contraction and increase in intracellular Ca^<2+> concentration ([Ca^<2+>]_i). However, pretreated with BQ-123 abolished ET-1-induced contraction and [Ca^<2+>]_i increase in renal artery. SNP, SNAP and forskolin reduced both ET-1-induced contraction and increase in [Ca^<2+>]_i in both pulmonary and renal arteries. However the effects were stronger in renal artery. ET-1-induced increase in [Ca^<2+>]_i was only partially attenuated by verapamil, whereas it reduced almost the half in renal arteries. ET-1-induced increase in [Ca^<2+>]_i in normal physiological salt solution (PSS) was reduced in Ca^<2+>-free PSS, and increase in [Ca^<2+>]_i of reapplication of CaCl_2 was not inhibited by nicardipine. Preincubation with Cyclopiazonic acid and thapsigargin inhibited ET-1-induced increase in [Ca^<2+>]_i in Ca^<2+>-free PSS, and also attenuated the ET-1-induced increase in [Ca^<2+>]_i. Phospholipase C (PLC) inhibitor U-73122 dramatically diminished both ET-1-induced increase in [Ca^<2+>]_i in Ca^<2+>-free PSS and subsequent application of CaCl_2. Treatment with 2APB and xestospongin C almost completely inhibit the induced increase in [Ca^<2+>]_i. Using RT-PCR, mRNA of TRPC1, TRPC4, TRPC5 TRPC6 and LTRPC7 were expressed in the tissue. These results demonstrate the presence of a receptor operated Ca^<2+>-influx controlled by downstream of PLC in the response of ET-1 in rat small pulmonary arteries.