Abstract
The concentrations of acetyl choline and acetyl cholinesterase were assayed in the brain, small intestine and kidneys of choline-deficient and supplemented weanling male Fischer rats. These measurements were made to explore our thesis that acute choline deficiency induces a deficiency in acetyl choline which makes the renal vasculature hyperresponsive to vasopressor amines, resulting in vasospasm, ischemia, vascular rupture, hemorrhage and renal tubular necrosis. We found that 5 days of choline deficiency resulted in a 30–35% decrease in the concentration of acetyl choline in the brain and small intestine and a 50–75% decrease in the kidney. The level of acetyl cholinesterase of the brain was unchanged; kidney acetyl cholinesterase was 18% lower in choline-deficient rats. These changes in tissue acetyl choline and acetyl cholinesterase levels occurred before there were changes in kidney weight and gross appearance or blood urea concentration. These experiments support our thesis that the nephropathy of acute choline deficiency results from vascular disturbances caused by a deficiency of acetyl choline.
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