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Journal of Nutrition Vol. 95 No. 4 August 1968, pp. 603-606
Copyright © 1968 by American Society for Nutrition
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Tissue Levels of Acetylcholine and Acetylcholinesterase in Weanling Germfree Rats Subjected to Acute Choline Deficiency1

Arnold L. Nagler2,3,, Wolf-D. Dettbarn4 and Stanley M. Levenson2

Small intestine and kidney acetylcholine levels were assayed in choline-deficient and normal weanling Fischer germfree (GF) and open-animal-room (OAR) rats to investigate our thesis that choline deficiency results in decreases in kidney acetylcholine making the renal vasculature hyperreactive to vasopressor amines, resulting in vasospasm, ischemia, vascular rupture, and tubular necrosis. We previously found that OAR rats develop much more severe nephropathy than GF rats when each are fed choline-deficient diets, due principally, we believe, to differences in choline metabolism and energy production. Accordingly, we postulated that renal acetylcholine levels should drop faster in choline-deficient OAR rats than in GF rats. We found that 5 days of dietary choline deficiency (a time before there are signs of nephropathy histologically or by blood urea concentration) resulted in decreased concentrations of acetylcholine in the small intestine (32%) and kidneys (40%) of OAR rats. There was no fall in kidney acetylcholine levels in the GF rats whereas the small gut acetylcholine level decreased 24%. Small intestine acetylcholinesterase levels of GF and OAR rats were similar and not affected by choline deficiency. These data are consistent with the above stated thesis regarding the pathogenesis of the nephropathy of choline deficiency.

1 Supported in part by grants 5 PO1 AM05664 (Germfree Research Program) and 5K5-GF-14,208 (Career Award, S. M. Levenson) from the National Institutes of Health to the Albert Einstein College of Medicine, Yeshiva University, New York, New York; also supported by grants NB 03304 and 1-K3-NB-Q5,133 (Career Award, W-D. Dettbarn) from the National Institutes of Health, and grant GB4844 from the National Science Foundation to the College of Physicians and Surgeons, Columbia University, New York.

2 Department of Surgery, Albert Einstein College of Medicine, Yeshiva University, New York.

3 Department of Pathology, Albert Einstein College of Medicine, Yeshiva University, New York.

4 Department of Neurology, The College of Physicians and Surgeons, Columbia University, New York.

Manuscript received 7 February 1968.




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