Hackenthal E, Lang R E, Bührle C P
Department of Pharmacology, University of Heidelberg, Federal Republic of Germany.
J Hypertens Suppl. 1985 Dec;3(3):S323-5.
Intrarenal infusion of atrial natriuretic factor has been reported to increase renal blood flow and sodium excretion, and either to depress or not to affect renin release. We examined the effect of a synthetic atrial peptide, AP II, on renin release, renal perfusate flow and glomerular filtration rate in isolated rat kidneys, perfused at constant pressure with a synthetic Krebs-Henseleit hydroxyethyl-starch-albumin medium. Atrial peptide II, 0.3 to 30 nmol/l, produced a concentration-dependent increase in renin release. Renal perfusate flow increased initially but returned to pre-infusion levels during infusion. During vasodilatation by continuous infusion of hydralazine, AP II produced only minor changes of perfusate flow but higher increases of renin release than in controls, indicating that this effect is not secondary to vasodilatation. During suppression of prostaglandin synthesis by indomethacin, the effects of AP II were unaltered. Furthermore, AP II in concentrations up to 200 nmol/l did not alter resting membrane potential in juxtaglomerular cells.
据报道，肾内注入心房利钠因子可增加肾血流量和钠排泄，并且对肾素释放有抑制作用或无影响。我们研究了一种合成心房肽AP II对离体大鼠肾脏肾素释放、肾灌注液流量和肾小球滤过率的影响，该肾脏在恒定压力下用合成的克雷布斯-亨塞尔特羟乙基淀粉-白蛋白培养基灌注。浓度为0.3至30 nmol/l的心房肽II可使肾素释放呈浓度依赖性增加。肾灌注液流量最初增加，但在灌注过程中恢复到灌注前水平。在通过持续输注肼苯哒嗪进行血管舒张期间，AP II仅使灌注液流量发生轻微变化，但肾素释放的增加幅度高于对照组，表明这种作用并非继发于血管舒张。在通过吲哚美辛抑制前列腺素合成期间，AP II的作用未改变。此外，浓度高达200 nmol/l的AP II不会改变球旁细胞的静息膜电位。
