Cantiello H F, Ausiello D A
Biochem Biophys Res Commun. 1986 Jan 29;134(2):852-60. doi: 10.1016/s0006-291x(86)80498-3.
The renal cell culture model, LLC-PK1, which contains an amiloride-sensitive conductive Na+ transport pathway and a Na+/H+ exchanger, was utilized to examine the direct effects of atriopeptin II and cGMP on Na+ transport in epithelial cells. Exposure of cells to atriopeptin II (10(-7) M) increased cGMP production within 2 min of addition to cells in monolayer. Atriopeptin II (10(-7) M) or exogenous 8-bromo-cGMP (10(-3) M) maximally inhibited the uptake of 22Na+ through the conductive pathway which accounted for up to 60% of total 22Na+ uptake. The apparent Ki for this inhibition by atriopeptin II was 2 X 10(-11) M. Amiloride inhibited 22Na+ uptake to a similar extent as atriopeptin II, and the effects of the presence of both agents was not additive. In contrast, neither atriopeptin II nor cGMP blunted the increment in 22Na+ uptake induced by a pH gradient. Thus atriopeptin II can directly inhibit Na+ transport in renal epithelial cells, probably through its stimulation of cGMP.
肾细胞培养模型LLC - PK1含有对氨氯吡咪敏感的传导性Na⁺转运途径和Na⁺/H⁺交换体，被用于研究心房肽II和环磷酸鸟苷（cGMP）对上皮细胞中Na⁺转运的直接作用。将细胞暴露于心房肽II（10⁻⁷M）中，在添加到单层细胞后的2分钟内cGMP生成增加。心房肽II（10⁻⁷M）或外源性8 - 溴环磷酸鸟苷（10⁻³M）最大程度地抑制了通过传导途径的²²Na⁺摄取，该传导途径占总²²Na⁺摄取量的60%。心房肽II这种抑制作用的表观抑制常数（Ki）为2×10⁻¹¹M。氨氯吡咪抑制²²Na⁺摄取的程度与心房肽II相似，且两种药物同时存在时的作用并非相加。相反，心房肽II和cGMP均未减弱由pH梯度诱导的²²Na⁺摄取增加。因此，心房肽II可能通过刺激cGMP直接抑制肾上皮细胞中的Na⁺转运。
