Locally produced dopamine (DA) causes a reversible and dose-dependent inhibition in Na+-K+-ATPase activity in rat proximal tubule (PT) segments [A. Aperia, A. Bertorello, and I. Seri. Am. J. Physiol. 252 (Renal Fluid Electrolyte Physiol. 21): F32-F45, 1987.]. To examine whether this effect might be of physiological importance, rats were given normal-salt (NS) or high-salt (HS) diet for 10 days. HS diet significantly increased Na excretion but did not alter glomerular filtration rate (GFR). Benserazide (Bz), an inhibitor of the enzyme L-aromatic amino acid decarboxylase (AADC) that converts L-dopa to DA, significantly attenuated the natriuresis in HS rats but had no effect on GFR. By use of immunofluorescence (IF) studies AADC was localized to the PT. Specific AADC IF was not observed in the medulla. In AADC-positive PT segments, Na+-K+-ATPase activity was significantly lower in HS rats than in NS rats (P less than 0.001). In AADC-negative medullary thick ascending limb, Na+-K+-ATPase activity was the same in NS and HS rats. If HS rats were given Bz just before study, PT Na+-K+-ATPase activity increased significantly and was not different from Na+-K+-ATPase activity in PT segments from NS rats. Bz had no significant effect on PT Na+-K+-ATPase activity in NS rats. In PT segments from Bz-treated rats, DA inhibited Na+-K+-ATPase activity already at a dose of 10(-8) M, whereas in segments from NS rats, significant inhibition of Na+-K+-ATPase activity was not observed until DA was increased to 10(-7) M.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of sodium nitrate were compared with sodium chloride loading on transport of electrolytes by the nephron. Maximal levels of free water clearance/clomerular filtration rate (CH2O/GFR) averaged 8.4% with nitrate loading and 14.4% with saline loading. Since ethacrynic acid and chlorothiazide exert their major natriuretic effect in the distal nephron, the increment in Na ad Cl reabsorbed beyond the proximal tubule. The administration of these agents resulted in an increase in fractional sodium excretion (CNa/GFR) of 21.1%, urinary sodium excretion (UNaV) of 1,126 mueq/min, and urinary chloride excretion (UClV) of 848 mueq/min during nitrate loading compared with an increase in CNa/GFR of 37.6%, UNaV of 2,362 mueq/min, and UClV of 2,397 mueq/min during saline loading. The smaller diuretic-induced increment in Na and Cl excretion in the nitrate studies suggests, as do the hydrated studies, that less Cl and Na are reabsorbed in the distal nephron during nitrate than saline loading. At every level of UNaV, fractional bicarbonate reabsorption was higher, urine pH was lower, and urinary potassium excretion (UKV) was higher in the nitrate studies. Thus, compared with saline loading, sodium nitrate decreases chloride and sodium reabsorption in the distal nephron. The higher hydrogen and potassium secretion in the nitrate studies may be consequent to the decreased ability of the distal nephron to reabsorb chloride.
The purpose of this study was to elucidate the mechanism whereby a potassium infusion led to an elevation in the urine minus blood (ohm-B) PCO2 difference in alkaline urine of the rabbit. Rabbits given 9alpha-fluorohydrocortisone 16 h prior to study had a significantly high olm-B PCO2 than control rabbits. However, the ohm-B PCO2 was increased further after potassium infusion. These results suggest that the increased collecting duct hydrogen ion secretion in the rabbit may in part have been induced by mineralocorticoids and in addition been influenced by increasing the potassium concentration.
There is a linear relationship between the PaCO2 and blood hydrogen ion concentration in normal dogs, but for theoretical reasons to be discussed, we questioned whether this relationship would apply in animals with metabolic acidosis or alkalosis. To study this in more detail, animals were divided into three groups: normal, metabolically acidotic, and metabolically alkalotic. Following anesthesia and bilateral ureteral ligation, dogs were intubated and ventilated to produce acute steady state PaCO2 values corresponding to the range observed during disease states. Changes in the volume and electrolyte composition of the gastrointestinal fluid and urine as well as the concentration and distribution of lactate were evaluated in all experiments. We observed the previously described linear relationship between the PaCO2 and blood hydrogen ion concentration in normal dogs, but the slope of the regression line differed significantly from those of dogs with metabolic acidosis and metabolic alkalosis. On the other hand, there was a consistent relationship between the ratio of the PaCO2 values, but not the absolute PaCO2, and the change in the plasma bicarbonate concentration over a wide range of PaCO2 values in all groups of dogs. The chemical basis for these observations will be discussed.
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