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首页> 外文期刊>Journal of Cellular Physiology >Dopamine stimulates 45Ca2+ uptake through cAMP, PLC/PKC, and MAPKs in renal proximal tubule cells.
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Dopamine stimulates 45Ca2+ uptake through cAMP, PLC/PKC, and MAPKs in renal proximal tubule cells.

机译：多巴胺刺激45 ca2 +吸收通过营地,PLC / PKC和MAPKs肾近端小管细胞。

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摘要

We have examined the effect of dopamine on Ca(2+) uptake and its related signaling pathways in primary renal proximal tubule cells (PTCs). Dopamine increased Ca(2+) uptake in a concentration (>10(-10) M) and time- (>8 h) dependent manner. Dopamine-induced increase in Ca(2+) uptake was prevented by SCH 23390 (a DA(1) antagonist) rather than spiperone (a DA(2) antagonist). SKF 38393 (a DA(1) agonist) increased Ca(2+) uptake unlike the case with quinpirole (a DA(2) agonist). Dopamine-induced increase in Ca(2+) uptake was blocked by nifedipine and methoxyverapamil (L-type Ca(2+) channel blockers). Moreover, dopamine-induced increase in Ca(2+) uptake was blocked by pertussis toxin (a G(i) protein inhibitor), protein kinase A (PKA) inhibitor amide 14/22 (a PKA inhibitor), and SQ 22536 (an adenylate cyclase inhibitor). Subsequently, dopamine increased cAMP level. The PLC inhibitors (U 73122 and neomycin), the PKC inhibitors (staurosporine and bisindolylmaleimide I) suppressed the dopamine-induced increase of Ca(2+) uptake. SB 203580 (a p38 MAPK inhibitor) and PD 98059 (a MAPKK inhibitor) also inhibited the dopamine-induced increase of Ca(2+) uptake. Dopamine-induced p38 and p42/44 MAPK phosphorylation was blocked by SQ 22536, neomycin, and staurosporine. The stimulatory effect of dopamine on Ca(2+) uptake was significantly inhibited by the NF-kappaB inhibitors SN50, TLCK, and Bay 11-7082. In addition, dopamine significantly increased the level of NF-kappaB p65, which was prevented by either SQ 22536, neomycin, staurosporine, PD 98059, or SB 203580. Thus, dopamine stimulates Ca(2+) uptake in PTCs, initially through by G(s) coupled dopamine receptors, PLC/PKC, followed by MAPK, and ultimately by NF-kappaB activation.
机译：我们已经检查了多巴胺对Ca(2 +)的影响吸收及其相关信号通路原发性肾近端小管细胞(ptc)。多巴胺增加Ca(2 +)吸收浓度(> 10(-10)米)和时间(> 8 h)依赖的方式。Ca(2 +)吸收是由原理图23390年预防(DA (1)拮抗剂)而不是spiperone (DA (2)拮抗剂)。增加Ca(2 +)吸收不同的情况quinpirole (DA(2)受体激动剂)。增加Ca(2 +)被吸收硝苯地平和methoxyverapamil (l型钙(2 +)通道阻滞剂)。增加Ca(2 +)被吸收百日咳毒素(G (i)蛋白抑制剂),蛋白激酶A (PKA)抑制剂酰胺(14/22PKA抑制剂)和22536平方(腺苷酸环化酶抑制剂)。营水平增加。和新霉素),PKC抑制剂(staurosporine我bisindolylmaleimide)镇压了由多巴胺带来的对增加Ca(2 +)吸收。203580 (p38 MAPK抑制剂)和PD 98059 (MAPKK抑制剂)也抑制了由多巴胺带来的对增加Ca(2 +)吸收。由多巴胺带来的对p38和p42/44 MAPK磷酸化被22536平方,新霉素,staurosporine。多巴胺对Ca(2 +)吸收的影响由NF-kappaB显著抑制SN50抑制剂TLCK,湾11 - 7082。此外,多巴胺显著增加了水平NF-kappaB p65,阻止了22536平方,新霉素,staurosporine PD203580年98059年,或某人。最初在ptc Ca(2 +)吸收,通过G (s)耦合的多巴胺受体,PLC / PKC,紧随其后的是MAPK,最终由NF-kappaB激活。

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