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R F Pitts

Publications and source records attributed to R F Pitts.

6 recordsLinked to original sources

Glutamine synthetase in kidneys of monkey and man.

1. The synthesis of gamma-glutamylhydroxamate from glutamate and hydroxylamine has been utilized as an approximation of glutamine synthetase activity in kidneys of rabbit, rat, dog, monkey and man. 2. Kidneys of rabbit contain glutamine synthetase in high activity; those of rat, in intermediate activity; and those of dog, monkey and man, in negligible activity. 3. No more enzyme is present in kidneys of the latter two species than in those of the dog, in which the enzyme is generally considered to be absent.

Animals

Action of phlorizin on luminal and antiluminal membranes of proximal cells of kidney.

In accord with results of others, we have observed that the infusion of phlorizin at low rates (2.16-117 microgram-kg-1-min-1) progressively increases fractional excretion of glucose from 0.47 to 0.85. Further increasing the rate of infusion to 2.19 mg-kg-1-min-1 increases fractional excretion to 1.0. The relationship appears to describe a single function having characteristics of an adsorption isotherm. The metabolism of the kidney, expressed as rate of total CO2 production from all substrates, is modestly and variably reduced by infusion of phlorizin at both high and low rates. The metabolism of glucose, expressed as rate of CO2 production, is variably but not consistently altered by infusion of phlorizin. The oxidation of [14C]lactate derived from [14C]glucose is negligible and introduces no significant error into measurement of 14CO2 from [14C]glucose. The percent of total CO2 derived from glucose does not differe significantly in control periods from the mean of all periods following phlorizin. Accordingly interaction of phlorizin with peritubular membranes at high rates of infusion, in the sense of blocking penetration of glucose, does not occur. Our methods do not rule out nor do they prove adsorption of phlorizin to these membranes.

Animals

Renal CO2 production from glutamine and lactate as a function of arterial perfusion pressure in dog.

The energy cost of renal function in the intact kidney of the dog was assessed at a series of arterial perfusion pressures. Pressure was varied by partially inflating a balloon at the tip of a catheter positioned in the aorta above the origins of the renal arteries. Either L-[U-14C]-lactate was infused intravenously in tracer amounts throughout each experiment. Total renal CO2 production and 14CO2 production from each isotope permitted assessment of total renal oxidative metabolism and the proportions derived from the two major substrates of the kidney. Stepwise inflation of the aortic balloon progressively lowered glomerular filtration rate, renal blood inflow, filtered and consequently reabsorbed Na+, total renal CO2 production, and 14CO2 derived from glutamine and lactate. The percent of total CO2 derived from lactate decreased more or less in proportion to the decrease in percent of total CO2 produced. Results were consistent with the view that reabsorption of sodium is the major energy sink of the kidney. They suggest that the oxidation of glutamine supplies energy for tubular transport and basal demands such as synthesis of hormones and maintenance of structure, whereas the oxidation of lactate supplies energy mainly for transport activities.

Acidosis

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History of Medicine

Metabolism of blood glucose by the intact functioning kidney of the dog.

The CO2 produced in the metabolism of blood glucose by the kidney has been measured by the i.v. infusion 14C-UL-D-glucose as a tracer. A small fraction of circulating 14C-glucose is converted to labeled lactate in extrarenal tissues, returned to, extracted by and metabolized to CO2 in the kidney. Correcting the apparent 14CO2 produced in the kidney from glucose for the 14CO2 produced from lactate yields that produced directly from glucose. Differences in production of CO2 from glucose in chronic metabolic acidosis and alkalosis are small and probably are not significant. If so, somewhat less than one-quarter of the total metabolism of the intact functioning kidney is supported by blood glucose. These measurements have been made at normal endogenous blood concentrations of glucose.

Acidosis