Unilateral renal infusion of acetylcholine resulted in diuresis on the infused side kidney, and antidiuresis were observed simultaneously on the contralateral (non-infused) side kidney. In this study, mechanism of diuretic effect of acetylcholine and antidiuretic effect of the contrala-teral side kidney were investigated employing clearance technique in 54 mongrel dogs under Nembutal anesthesia. Almost experiments were performed by dehydrated dogs, and in some experiments, hydrated dogs were used for analysis of tubular site of action of acetylcholine. 1. Under dehydration, diuretic effect of acetylcholine was accompanied with increased non-cortical plasma flow and tubular rejektion fraction of Na, but has no dependence on GFR and effective renal plasma flow. TH2O declined to zero and CHZp was detected by administration of Acetylcholine, meaning of inhibition of Na reabsorption by the distal tubule. Under hydration, fractional CH2O and fractional Cosm showed parallel increase, suggesting an inhibition of Na reabsorption by the proximal tubule. That is, acetylcholine inhibits water and Na reabsorption in the proximal and distal tubules, and under dehydration, increased medullary circulation may in part have a role of diuretic effect. 2. On the contrary, non-infused side kidney, urine volume decreased with decrement of effective renal plasma flow. After unilateral renal denervation, antidiuresis on the contralateral side induced by acetylcholine cannot be observed, suggesting an exisistence of neural reflex between two kidneys (Reno-Renal Reflex.) It is known that renal afferent nerves are activated by the elevation of renal venous pressure. Unilateral renal infusion of acetylcholine may stimulate the pressure receptor by an increase of medullary circulation and may evoke the afferent impulse. This impulse is mediated to the contralateral efferent nerves and this, in turn, decrease effective renal plasma flow, then secondary decrease urine volume on the contralateral side.

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In order to investigate renal metabolism in chronic renal failure, the enzyme activities of TCA cycle and some others were measured in human contracted kidney. To study the cause of the changes of the enzyme activities in human contracted kidneys, the enzyme activities of TCA cycle and some others were measured in histologicaIly disturbed rabbit kidneys treated by uranium nitrate, ishcemic rabbit kidneys treated by the renal artery stenosis operation and the rabbit kidneys perfused by ultrafiltrate from the serum of uremic patients. Furthermore, the extra corporeal perfusion experimentation by ultrafiltrate from uremic patients was carried out, in which PSP cxcreation in urine was calculated in order to examine the relation between the renal tubule active transport and the abnormality of body fluids in renal failure. The results are as follows, 1) The activities of all the TCA cycle enzymes (ICDH, SuDH, MDH and GL-DH) and the LDH activity decrease in renal cortex, medulla and papilla of human contracted kidneys. 2) The activities of enzymes written above all decrease in renal cortex, medulla and papilla of human contracted kidneys. 3) The activities of enzymes written above all decrease in rabbit kidneys treated by uranium nitrate. 4) In the ischemic rabbit kidneys, the decrease of enzyme activity is observed. And the decrea-sing rate is larger than in the rabbit kidneys treated by uranium nitrate. 5) The activities of ICDH, SuDH, MDH and GL-DH decrease and the LDH activity increases in the rabbit kidneys perfused by ultrafiltrate from uremic patients. 6) It seems that a certain substance, causing the lowering of PSP excretion from tubule, is con-tained in ultrafiltrate from the serum of uremic patients. 7) From the results above, it is assumed the decrease of enzyme activity in human contracted kidneys is related to the three elements-destroyed renal tissue, renal ischemia and abnomal serum meta-bolites and that the renal tubular function is related closely to the decrease of the enzyme activities.

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