Relationship between body mass, tissue metabolic rate, and sodium pump activity in mammalian liver and kidney

The allometric relationship between body mass and tissue metabolism was examined in liver and kidney cortex slices from mouse, rat, rabbit, sheep, and cattle, representing an approximately 12,000-fold difference in body mass and an 11-fold difference in mass-specific basal metabolic rate. Larger mammals have lower tissue metabolic rates (TMR; mumol O2.g wet wt-1.min-1) at 37 degrees C, yielding the equations TMR = 3.6 M-0.21 for liver slices and TMR = 3.2 M-0.11 for kidney cortex slices, where M is body mass in grams. This appears to be an intrinsic property of the tissue and is not due to differences in extracellular space or tissue protein content, because these are relatively constant in all mammalian species examined. The allometric relationships remain when tissue metabolism is expressed relative to "active cell mass" in tissue slices. Potassium uptake rate (KUR; mumol K+.g wet wt-1.min-1) was also measured (as 86Rb+ uptake) and was also lower in larger mammals, yielding the equations KUR = 1.2 M-0.14 in liver slices and KUR = 3.4 M-0.13 for kidney cortex slices. The energetic costs of sodium pump activity were estimated to be < 10% of TMR for liver and kidney cortex from all five mammalian species.

Tamm—Horsfall Glycoprotein Release from Rat Kidney Cortex Slices in Vitro

1. Rat kidney cortex slices were incubated for 30 min at 37°C in unmodified Krebs-Henseleit buffer containing aldosterone, vasopressin, theophylline, ethacrynic acid, frusemide, spironolactone or ouabain. 2. Tamm—Horsfall glycoprotein (THG) released into the media was measured by radioimmunoassay and at the end of each experiment the slices were homogenized and assayed for THG content. 3. Incubation of kidney cortex slices in unmodified buffer resulted in a significant increase in the slice THG content when compared with pre-incubation levels. The increase was prevented by puromycin or cycloheximide. 4. Incubation in ethacrynic acid (1 mmol/l) or frusemide (10 mmol/l) resulted in a significant increase in release of THG when compared with unmodified buffer. Puromycin or cycloheximide failed to prevent the increased release. 5. THG release induced by ethacrynic acid or frusemide is probably the result of an aggregation-disaggregation reaction on the cell membrane. It is suggested that the action of the chloride inhibiting diuretics, ethacrynic acid and frusemide, is mediated in some way via THG.