EFFECTS OF ENDOTHELIUM-DERIVED NITRIC-OXIDE ON RENAL HEMODYNAMICS ANDFUNCTION IN THE SHEEP FETUS

Citation
Ga. Bogaert et al., EFFECTS OF ENDOTHELIUM-DERIVED NITRIC-OXIDE ON RENAL HEMODYNAMICS ANDFUNCTION IN THE SHEEP FETUS, Pediatric research, 34(6), 1993, pp. 755-761
Citations number
57
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00313998
Volume
34
Issue
6
Year of publication
1993
Pages
755 - 761
Database
ISI
SICI code
0031-3998(1993)34:6<755:EOENOR>2.0.ZU;2-A
Abstract
We investigated the effects of the endothelium-derived nitric oxide sy stem on renal hemodynamics and function during the 3rd trimester in a chronically catheterized fetal sheep preparation. Acetylcholine caused a significant decrease in renal vascular resistance (60% of the basel ine value) as compared with aortic constriction (142% of the baseline value). The effects of acetylcholine could be blocked by prior adminis tration of N(omega)-nitro-L-arginine (renal vascular resistance = 102% of baseline). Sodium nitroprusside also caused a significant drop in renal vascular resistance (63% of baseline), but this could not be blo cked by N--nitro-L-arginine (77% of baseline). Infusion of N--nitro-L- arginine with blood pressure maintained at a constant level resulted i n a significant increase in renal vascular resistance (148% of the bas eline value) as compared with saline alone (94% of baseline). Glomerul ar filtration rate increased after saline infusion (156% of the baseli ne value), but this increase was blocked by N(omega)-nitro-L-arginine (87% of baseline). Sodium excretion also increased (340%), and this in crease was blunted by N(omega)-nitro-L-arginine (235%). We conclude th at basal production of endothelium-derived nitric oxide results in ong oing renal vasodilation in 3rd-trimester fetal sheep, maintaining base line renal blood flow. The endothelium-derived nitric oxide system can also be stimulated to an increased level of activity, and its blockad e partially prevents the homeostatic response of the fetus to volume a nd salt overload.