Kurtz A, Della Bruna R, Pfeilschifter J, Bauer C
J Hypertens Suppl. 1986 Jun;4(2):S57-60.
We examined the effect of synthetic atrial natriuretic peptide (ANP) on unstimulated renin release from rat renal juxtaglomerular cells. Using renal cortical cell cultures containing 80-90% juxtaglomerular cells, we found that ANP strongly inhibited renin release from the cells in a dose-dependent fashion. Half-maximal inhibition was observed at 10(-11) mol/l ANP. Furthermore, ANP produced a rise in the intracellular concentration of cyclic guanosine monophosphate (cGMP) and a fall in the concentration of cyclic adenosine monophosphate (cAMP). Data indicated that the inhibition of renin release by ANP was related to the rise in cGMP and not to the fall of cAMP. Atrial natriuretic peptide (10(-10) mol/l) had no influence on the transmembrane calcium influx nor did it alter the intracellular calcium concentration of the juxtaglomerular cell. We found, however, that the inhibitory effect of ANP on renin release could be attenuated by the calcium channel blocker verapamil. Our results suggest that ANP inhibits renin release from juxtaglomerular cells by a mechanism that is mediated by cGMP; the mechanism is not linked to any alteration in intracellular calcium concentration but requires a normal level of calcium.
我们研究了合成心房利钠肽（ANP）对大鼠肾近球细胞未受刺激时肾素释放的影响。利用含有80 - 90%近球细胞的肾皮质细胞培养物，我们发现ANP以剂量依赖方式强烈抑制细胞的肾素释放。在10^(-11) mol/L的ANP浓度下观察到半数最大抑制。此外，ANP使细胞内环磷酸鸟苷（cGMP）浓度升高，环磷酸腺苷（cAMP）浓度降低。数据表明，ANP对肾素释放的抑制与cGMP的升高有关，而非与cAMP的降低有关。心房利钠肽（10^(-10) mol/L）对跨膜钙内流无影响，也未改变近球细胞的细胞内钙浓度。然而，我们发现钙通道阻滞剂维拉帕米可减弱ANP对肾素释放的抑制作用。我们的结果表明，ANP通过一种由cGMP介导的机制抑制近球细胞的肾素释放；该机制与细胞内钙浓度的任何改变无关，但需要正常水平的钙。
