Mulvany M J, Aalkjaer C, Juul B, Nyborg N C, Andresen J
Biophysics Institute, Aarhus University, Denmark.
J Hypertens Suppl. 1985 Dec;3(3):S307-9.
The action of a synthetic 'atrial natriuretic factor' (sANF) on induced tone in isolated rat renal resistance vessels (lumen diameter about 200 microns) was examined and compared with the effects of sANF on resistance vessels of similar size taken from the cerebral, mesenteric and femoral vasculature. Synthetic ANF caused a relaxation of the renal vessels when these were submaximally activated with noradrenaline or serotonin, but had no effect on the responses of the other vessels to these agonists. In contrast to previous reports concerning rabbit aortic vessels, methylene blue (which is thought to cause inhibition of guanyl cyclase) did not reduce the dilator response to sANF in the renal vessels. The results demonstrate that sANF has a specific relaxing effect on renal resistance vessels, and are consistent with its effect being mediated through specific receptors. The mechanism of this relaxant effect remains unknown.
研究了合成的“心房利钠因子”（sANF）对离体大鼠肾阻力血管（管腔直径约200微米）诱导张力的作用，并将其与sANF对取自脑、肠系膜和股部血管系统的类似大小阻力血管的作用进行了比较。当用去甲肾上腺素或5-羟色胺使肾血管亚最大程度激活时，合成的ANF可使其舒张，但对其他血管对这些激动剂的反应无影响。与先前关于兔主动脉血管的报道相反，亚甲蓝（被认为可抑制鸟苷酸环化酶）并未降低肾血管对sANF的舒张反应。结果表明，sANF对肾阻力血管具有特异性舒张作用，且与其通过特异性受体介导的作用一致。这种舒张作用的机制尚不清楚。
