Alteration of renal hemodynamic in adriamycin-induced nephrosis rats administrated with Wulingsan.
- Author:
Lan HE
1
;
Yu CAI
;
Zhao-Hui CHEN
;
Jian-Min JIANG
;
Ning-Sheng WANG
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; metabolism; Animals; Doxorubicin; Drugs, Chinese Herbal; isolation & purification; pharmacology; Endothelins; metabolism; Glomerular Filtration Rate; drug effects; Kidney; metabolism; physiopathology; Male; Medicine, Chinese Traditional; Nephrosis; chemically induced; metabolism; physiopathology; Nitrous Oxide; metabolism; Plant Extracts; pharmacology; Plants, Medicinal; chemistry; Rats; Rats, Sprague-Dawley; Renal Circulation; drug effects; Renal Plasma Flow; drug effects; Vascular Resistance; drug effects
- From: China Journal of Chinese Materia Medica 2006;31(16):1358-1360
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of traditional classical compound Wulingsan on renal hemodynamic in rats with adriamycin (ADR)-induced nephrosis.
METHODAfter establishing a model of rats with adriamycin-induced nephrosis, we administrated wulin-san to the ADR rats via oral gavage for four weeks and measured mean arterial blood preasure (MABP) with manometer. Renal clearance of paraaminohippuric acid (PAH) and inulin were detected, then renal plasma flow (RPF) and glomerular filtration rate (GFR) were calculated. Renal vascular resistance (RVR) was calculated as the division of MABP by RPF. Renal endothelin (ET) and angiotensin II (Ang II) were detected with radioimmunity assay kits, and nitrous oxide (NO) was detected with biochemical kits.
RESULTThere was no significant change of GFR in ARD rats, but RPF and NO were decreased, which accompanied by enhanced RVR, ET and Ang II. RPF was increased in the administrated rats, in company with RVR, ET and Ang II decreased, whereas NO was not influenced after the administration.
CONCLUSIONWulingsan can improve the renal hemodynamic in ADR rats, at least in part by modulating the levels of vasoactive factor.