Mechanisms of proximal proton secretion in BBM of herbivorous, omnivorous, and carnivorous species.

The mechanisms of proton secretion by the proximal brush-border membrane (BBM) were compared in carnivorous (dog), omnivorous (human, pig, rat), and herbivorous (rabbit, hamster) species. The activity of the proton pump (V-type bafilomycin-sensitive H(+)-adenosinetriphosphatase) and of the Na+/H+ exchanger (amiloride-sensitive quenching of acridine orange fluorescence), the two major proton secretion mechanisms, was measured. The enzymatic activity of the H(+)-adenosinetriphosphatase activity was measured in intact (endosomes) and solubilized (0.

Cross-talk between the Na(+)-K(+)-ATPase and the H(+)-ATPase in proximal tubules in suspension.

The cellular energy required for the activity of the Na(+)-K(+)-ATPase and of the H(+)-ATPase was estimated in intact proximal tubules in suspension. Both the fall in oxygen consumption (directly measured) and NADH oxidation (as estimated from exogenous substrate metabolism) were measured before and following application of ouabain (1 mM) to inhibit the sodium pump, following bafilomycin (0.1 mM) to inhibit the proton pump or following a combination of these inhibitors.

Basolateral membrane potassium channels in rabbit cortical thick ascending limb.

The nature of K exit across the basolateral membrane of rabbit cortical thick ascending limb (CTAL) was investigated using the patch clamp technique. The basolateral membrane was exposed by mild collagenase treatment (0.1 U/ml), and a K-selective inwardly rectifying channel was identified.

Intracellular potassium activity in mammalian proximal tubule: effect of perturbations in transepithelial sodium transport.

Intracellular potassium activity (alpha Ki) was measured in control conditions in mid-cortical rabbit proximal convoluted tubule using two methods: (i) by determination of the K+ equilibrium potential (EK) using Ba(2+)-induced variations in the basolateral membrane potential (VBL) during transepithelial current injections and (ii) with double-barrel K-selective microelectrodes. Using the first method, the mean VBL was -48.5 +/- 3.

Regulation of basolateral membrane potential after stimulation of Na+ transport in proximal tubules.

We have previously shown that stimulation of apical Na-coupled glucose and alanine transport produces a transient depolarization of basolateral membrane potential (Vbl) in rabbit proximal convoluted tubule (PCT, S1 segment). The present study is aimed at understanding the origin of the membrane repolarization following the initial effect of addition of luminal cotransported solutes. Luminal addition of 10-15 mM L-alanine produced a rapid and highly significant depolarization of Vbl (20.

Maleate-induced stimulation of glutamine metabolism in the intact dog kidney.

Studies were performed in anesthetized normal dogs to evaluate the effects of maleate on renal metabolism. Intravenous administration of maleate (50 mg/kg) markedly increased urinary excretion of glutamine, glutamate, alpha-ketoglutarate, alanine, lactate, pyruvate, and citrate. Despite a fourfold rise in renal cortical concentration of alpha-ketoglutarate, glutamine utilization expressed per 100 ml glomerular filtration rate almost doubled following maleate administration, whereas total ammonia production increased threefold, most of this ammonia being diverted into the renal vein.

Renal metabolism and ammoniagenesis during acute respiratory alkalosis in the dog.

Acute respiratory alkalosis (blood pH, 7.60; arterial PCO2, 15 mmHg (1 mmHg = 133.322 Pa); plasma bicarbonate, 14 mM) was induced in nine anesthetized dogs by increasing their respiratory rate and depth.

Bicarbonaturic effect of acetazolamide in the dog: the influence of graded volume expansion.

Studies were performed in anesthetized dogs to characterize the effect of a progressive volume expansion on the acetazolamide-induced bicarbonaturia. A closed system with urine reinfusion was used in all these experiments. In normovolemic dogs, 24% of the filtered bicarbonate was excreted into the urine while this value reached 62% when a 10% expansion was superimposed on a continuous infusion of acetazolamide.

Immediate adaptation of the dog kidney to acute hypercapnia.

Studies were performed to determine whether ammoniagenesis could adapt instantaneously to acidosis in the dog kidney. Following acute respiratory acidosis, renal glutamine extraction rose acutely in dogs with stable renal blood flow but did not change when the renal blood flow fell by more than 25%. Acute hypercapnia immediately increased renal ammonia production in both groups of dogs.