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M Acara

Publications and source records attributed to M Acara.

11 recordsLinked to original sources
PubMed1979

Isoproterenol excretion and metabolism in the isolated perfused rat kidney.

[3H]isoproterenol excretion and metabolism were studied in the isolated perfused rat kidney using a one-pass, non-recirculating perfusion system with constant infusion rates of [3H]isoproterenol. The [3H]isoproterenol (U/P) to inulin (U/P) ratio was approximately 15 indicating extensive tubular secretion. A major renal metabolite, 3-O-methylisoproterenol, appeared in the urine and renal vein perfusate and also accumulated in the renal tissue. The fractional excretion of isoproterenol decreased with time while fractional excretion of p-aminohippurate remained stable. The observed decreasing urinary clearance and percent extraction of isoproterenol with time may be due to the progressive intrarenal accumulation of 3-O-methylisoproterenol.

Animals↗
PubMed1977

Relations of renal transport rate, transport maximum, and competitor potency for tetraethylammonium and choline.

By use of the Sperber technique in chickens, the renal tubule transport maximum (Tm) for the organic cation tetraethylammonium (TEA) was determined in vivo. The tubular transport rate, the Tm, and the competitor potency are assumed to have causal relationships. It was demonstrated that the two cations TEA and choline compete for the tubular transport of [14C]TEA. The saturating load of one cation was reduced by the simultaneous presence of the other. The Tm for these two cations was different by a factor of 2.4 and their respective competitor potency was inversely related to their Tm.

Animals↗
PubMed1976

Choline loss during hemodialysis: homeostatic control of plasma choline concentrations.

Endogenous concentrations of free choline in plasma were measured in azotemic subjects receiving repetitive hemodialysis and excretion of free choline into the dialysate was determined. Chemical choline in plasma and dialysate was measured by adding choline kinase and measuring the production of radiolabelled phosphorycholine in the presence of radiolabelled adenosine triphosphate (ATP). Mean free choline concentration in plasma of azotemic subjects receiving hemodialysis was found to be 37 muM, which is about twice that of normal persons. The total excretion of choline into the dialysate during 360 min averaged 730 mumoles +/- 69 (SEM). Levels of free choline in plasma fell during hemodialysis at two hours but recovered toward predialysis values at six hours. The return of plasma choline concentrations toward control values during dialysis suggests that a feedback mechanism exists which was activated rapidly to produce homeostasis of plasma choline concentrations. In these patients, the degree of peripheral neuropathy as judged by measurement of nerve conduction velocities showed a significant inverse correlation with levels of free choline in plasma.

Blood Flow Velocity↗
PubMed1976

The biphasic effect of organic cations on the excretion of other organic cations.

The renal excretion of 14C-choline or 14C-acetylcholine was increased by the infusion of another organic cation at low rates but was decreased by infusion of the same added organic cation at higher rates with the Sperber technique in hens. The range of low rates of infusion was from 1 X 10(-15) to 1 X 10(-8) mol/min. At infusion rates greater than 1 X 10(-8) mol/min, inhibition of tubular excretion was found. At the low infusion rates, thiamine, lysine, quinine, atropine, acetylcholine and methylguanidine were found to increase 14C-choline excretion. The same compounds with the exception of lysine and acetylcholine inhibited 14C-choline excretion at the higher infusion rates. A biphasic effect on 14C-acetylcholine excretion was also observed with added atropine, thiamine and choline over the same infusion range. Increases in 14C-choline excretion occurred during a choline infusion rate that normally produced an excretory tubular maximum for choline whereas increases in 14C-acetylcholine excretion occurred during infusion of tracer amounts of 14C-acetylcholine. The effect of the addition of organic cations was selective for cations since the tubular excretion of organic anions was not affected by the addition of organic cations. The tubular excretion ratio of 14C-thiamine/p-aminohippuric acid increased from 0.25 to 0.95 when the infusion rate of added unlabeled thiamine was increased from 1 X 10(-11) to 1 X 10(-8) mol/min. Enhanced tubular excretion of 14C-thiamine may represent the effect of the increased load of unlabeled thiamine to protect the labeled thiamine from conversion to a nontransportable metabolite. Enhancement of excretion of 14C-choline and 14C-acetyocholine produced by very small amounts of other organic cations may represent either inhibition of tubular reabsorptive transport or induction of tubular excretory transport.

Acetylcholine↗
PubMed1975

Renal tubular excretion of triethylcholine (TEC) in the chicken: enhancement and inhibition of renal excretion of choline and acetylcholine by TEC.

1. [3H]-triethylcholine (TEC) was actively transported by the renal tubule of the chicken at a rate 85% that of simultaneously administered p-aminohippuric acid (PAH). 2. TEC was demonstrated to be transported by the organic cation transport system in the kidney through inhibition with quinine and the bio-cation choline. 3. When the infusion of TEC was increased to 2 times 10(-6) mol kg(-1) min(-1) reaching the infused kidney, the transport of [3H]-TEC was inhibited, suggesting that an excretory transport maximum for TEC in the renal tubules had been reached. 4. The excretion of both choline and acetylcholine was enhanced by TEC loads as low as 1 times 10(-18) mol kg(-1) min(-1). Enhancement continued as TEC infusion was increased up to approximately 1 times 10(-7) mol kg(-1) min(-1) at which point this enhancement was converted to inhibition. 5. Possible mechanisms for the biphasic effect of TEC on organic cation transport are discussed.

Acetylcholine↗
PubMed1975

The kidney in regulation of plasma choline in the chicken.

Exogenous choline was administered into the wing vein of chickens until steady-state plasma choline levels were achieved. Both plasma and urine were analyzed for free choline by a choline kinase, radiochemical microassay that did not require prior extraction of choline from the biological fluids. Choline was infused at rates from 0.5 to 20.0 mumol/kg-min. Total and urinary clearance were assessed at the steady state reached in each experiment. At the endogenous level of plasma choline of 0.019 mM, total clearance of choline from the plasma was about 50 ml/kg-min and urinary clearance was 0.06 ml/kg-min. There was no significant increase in urinary clearance of choline produced by infusion loads from 0.5 to 1.0 mumol/kg-min. However, as the infusion of choline was increased further, extraurinary clearance decreased while the contribution of the kidneys to total clearance of choline from the plasma increased. At the choline infusion rate of 12.5 mumol/kg-min, plasma choline was 0.5 mM and urinary choline clearance had reached a maximum value of 18.5 ml/kg-min for two kidneys, removing more than 70% of the infused choline.

Animals↗
PubMedDate not supplied

Renal N-oxidation of trimethylamine in the chicken during tubular excretion.

The Sperber technique of infusion into the renal portal circulation in chickens was used to investigate in vivo the renal tubular transport and renal metabolism of trimethylamine (TMA). When 14C-TMA was infused at a rate of 1 x 10(-9) mol/min the transport efficiency (TE), that is, the tubular excretion of the 14C-label relative to excretion of simultaneously infused paminohippuric acid, was 0.70. Progressive addition of unlabeled TMA up to infusion rates of 1 x 10(-5) mol/min produced a progressive fall in the TE of the 14C-label. Identification of the 14C-label excreted in the urine revealed that approximately 85% of the infused 14C-TMA was excreted by the infused kidney as a single metabolite over the entire range of infusions. By use of the techniques of low-voltage electrophoresis, high-voltage electrophoretic mobility-pH profile, and gas chromatography/mass spectrometry, the renal metabolite was found to be identical with standard 14C-trimethylamine oxide (TMAO). At a TMA infusion rate of 1.5 x 10(-6) mol/kg/min reaching the infused kidney, the rate at which TMAO was formed and excreted by the kidney was 0.12 x 10(-6) mol per g of kidney per min. When 14C-TMAO was infused into chickens its TE was 0.11, which was not evidence for active excretory transport. Infused TMA was almost entirely metabolized in vivo to its N-oxide, TMAO, which then entered the urine. The renal tubular excretion of 14C during infusion of 14C-TMA was inhibited by the cationic blocker of transport, quinine, and by the anionic blocker of transport, probenecid.

Animals↗
PubMedDate not supplied

Effect of ethanol on the renal excretion and metabolism of choline in the isolated perfused rat kidney.

The isolated perfused rat kidney was used to investigate the effect of ethanol on the renal excretion and metabolism of choline. Choline at an initial perfusate concentration of 2.8 mM, with tracer amounts of [methyl-14C]choline, was recirculated through kidneys and radioactivity measured in perfusate, urine, and kidney. 14C-Choline and its metabolites were identified by chromatographic and electrophoretic procedures. Tubular excretion of choline was demonstrated and a transport maximum (Tm) of 1.6 mumol/kidney/min was reached at a choline perfusate concentration of 1.2 mM. Addition of 50 mM ethanol resulted in a 56% increase in the choline Tm and 100 mM ethanol decreased the choline Tm by 25%. The rate of loss of 14C-choline from the perfusate was increased by the lower ethanol concentration and decreased by the higher ethanol concentration. Ethanol at both concentrations diminished the amount of 14C remaining in the kidney. 14C-Betaine was the major choline metabolite and the only 14C-metabolite present in perfusate or urine. Addition of either 50 or 100 mM ethanol increased both glomerular filtration rate and urine volume.

Animals↗