Effects of Acetylcholine on the Renal Function in Renal Hypertensive Rabbits.
- Author:
Seung Moo NOH
1
;
Suhn Hee KIM
;
Kyung Woo CHO
Author Information
1. Deparment of General Surgery, College of Medicine, Chungnam National University, Daejun, Korea. kwcho@moak.chonbuk.ac.kr
- Publication Type:Original Article
- Keywords:
Acetylcholine;
Nitric oxide;
Rabbit;
Renal function;
Renal hypertension
- MeSH:
Acetylcholine*;
Endocrine Glands;
Endothelium, Vascular;
Filtration;
Hemodynamics;
Hypertension, Renal;
Kidney;
NG-Nitroarginine Methyl Ester;
Nitric Oxide;
Rabbits*;
Renal Plasma Flow;
Water
- From:Korean Journal of Nephrology
2000;19(6):1012-1023
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
It has long been known that acetylcholine infusion resulted in increases in urine volume, urinary excretion of Na and renal plasma flow. Exact mechanism of renal effects of acetylcholine, however, has not yet been clarified. Since the discovery of endothelium-derived relaxing factor/nitric oxide system, the vascular endothelium has been considered as an endocrine gland. The purpose of the present study was to define the effect of acetylcholine on the renal hemodynamic and tubular function, and the modification of the renal effects of acetylcholine in two- kidney one clip Goldblatt hypertensive rabbits. Intrarenal acetylcholine(0.03-0.3ug/kg/min) increased glomerular filtration rate(GFR, CCr), renal plasma flow (RPF, CPAH), urine volume(UV), free water clearance (CH2O), urinary excretion of electrolytes(UNaV, UKV) and nitrate(UNO3V) and fractional excretion of Na+ (FENa) in unanesthetized rabbits. No change in filtration fraction was observed. Pretreatment with N omega- nitro-L-arginine methyl ester(L-NAME) blocked the acetylcholine-induced renal effects. Acetylcholine infused into the contralateral kidney elicited increases in GFR, RPF, UV, CH2O, UNaV, UKV, UNO3V and FENa in hypertensive rabbits. The hemodynamic effect was not different between normotensive sham-operated and unilateral nephrectomized rabbits. Acetylcholine-induced tubular effect, however, was significantly accentuated in hypertensive rabbits. Neither the renal hemodynamic nor tubular effects of acetylcholine were observed with pretreatment of L-NAME. These results suggest that the renal tubular effect as well as hemodynamic effect of acetylcholine is mediated through the NO system and that the tubular effect of acetylcholine is accentuated in the early phase of renal hypertension.
