Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ALKALOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1992

Metabolic alkalosis as driving force for urea synthesis in liver disease: pathogenetic model and therapeutic implications.

Despite a marked reduction of the urea cycle capacity, patients with well-compensated chronic liver disease excrete near-normal amounts of urea. Compensation of the urea cycle defect apparently occurs through the activation of liver glutaminase, as suggested by an inverse relationship between the in vitro ureagenic capacity and the flux through glutaminase in liver tissue from patients with a normal, fatty, or cirrhotic liver. In these patients, the flux through glutaminase, as determined in vitro, increases in parallel with the plasma bicarbonate level and plasma pH determined in vivo. In view of this and results from previous studies, the following hypothesis is suggested: The decrease of urea cycle enzyme activities in liver cirrhosis produces metabolic alkalosis due to an impaired bicarbonate elimination. Alkalosis in turn activates and stabilizes hepatic glutaminase and accordingly mitochondrial ammonia provision for carbamoylphosphate synthetase. This results in a compensatory stimulation of the urea cycle flux in the cirrhotic patient to near-normal rates, despite the marked reduction of urea cycle enzyme activity. Accordingly, alkalosis is an important driving force for urea synthesis in the cirrhotic patient. With respect to clinical medicine, attention must be paid to acid-base disturbances in the hyperammonemic patient.

Alkalosis↗
PubMed1985

Influence of respiratory acidosis or alkalosis on pressor responses mediated by alpha 1- and alpha 2-adrenoceptors in pithed normotensive rats.

The effect of respiratory acidosis and alkalosis on the vasoconstriction to alpha 1- and alpha 2-adrenoceptor stimulation was studied in pithed normotensive rats. The selective alpha 1-adrenoceptor agonists (-)amidephrine, cirazoline, (+/-)erythro methoxamine, (-)phenylephrine, Sgd 101/75 and St 587 were used, as well as the selective alpha 2-adrenoceptor agonists B-HT 920, B-HT 933, DP-6,7-ADTN, M-7 and UK 14,304. The non-selective alpha-adrenoceptor agonists xylazine, noradrenaline and adrenaline were included as well. The latter two were also studied under selective doses of the antagonists rauwolscine and prazosin, thus yielding the respective alpha 1- and alpha 2-adrenoceptor components of the vasoconstriction to these agonists. The effect of acid-base balance disturbances on presynaptically released noradrenaline elicited by electrical stimulation of preganglionic nerves was studied as well. Dose response curves for the agonists were generated under various conditions of ventilation, yielding either alkalotic, normal or acidotic values of arterial blood pH. Pressor responses to all agonists were maximally affected by changes in acid-base status at the low doses of the agonists. Acidosis was found to inhibit increases in diastolic pressure mediated by the alpha 1-as well as the alpha 2-adrenoceptor agonists studied, although not to the same extent. Alkalosis exerted either an obvious potentiation or did not significantly influence alpha 1-adrenoceptor mediated pressor responses. On the basis of acid-base sensitivity the following groups of agonists were distinguished: Cirazoline, phenylephrine, methoxyamine, electrically released noradrenaline from presynaptic sites, of which pressor responses are obviously potentiated and attenuated by alkalosis and acidosis, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1991

Cystic fibrosis presenting with recurrent vomiting and metabolic alkalosis.

Between January 1980 and December 1987, ten Saudi Arabian children at Saudi Arabian Oil Co. (Saudi Aramco) health care facilities in the Eastern Province of Saudi Arabia had cystic fibrosis (CF). The incidence of CF in Saudi Arab children less than or equal to 14 years was 1 in 4243. Five of the ten children had hypoelectrolytaemia and metabolic alkalosis on initial presentation. Two of the five had recurrent vomiting, hypoelectrolytaemia and metabolic alkalosis alone and initially no chest symptoms. Early exclusion of CF should be part of the workup in any child, especially in an infant with hypoelectrolytaemia and metabolic alkalosis.

Alkalosis↗
PubMed1996

The effects of induced alkalosis on the metabolic response to prolonged exercise in humans.

To examine the effects of alkalosis on the metabolic response to prolonged exercise, seven healthy males cycled for 1 h at approximately 70% of maximum oxygen uptake on two occasions, 1-week apart. Starting 3 h prior to exercise, subjects consumed either CaCO3 (placebo) or NaHCO3 (0.3 g.kg-1 body mass) over a 2-h period. Arterialised-venous blood samples were drawn before and during exercise for the determination of acid-base status and blood metabolites (lactate, glucose, glycerol and plasma free fatty acids). Expired gas was collected during exercise for determination of oxygen uptake (VO2) and respiratory exchange ratio to estimate fuel oxidation rates. Ratings of perceived exertion (RPE) and heart rates were also recorded. A significant (P < 0.01) alkalosis was observed at all times following bicarbonate ingestion. Blood lactate was significantly (P < 0.05) higher at all sample times throughout exercise following bicarbonate ingestion. Blood lactate concentration [mean (SEM)] reached peak values of 2.90 (0.16) and 4.24 (0.45) mmol.l-1 following 20 min of exercise following placebo and bicarbonate, respectively. No differences between treatments were noted at any time for the other metabolites. VO2 and RPE were significantly higher (P < 0.01) with the bicarbonate trial. At a constant power output increases in VO2 are generally associated with increases in fat oxidation, however, no evidence for an altered fuel oxidation was obtained in the present study. The differences in blood lactate indicate that induced alkalosis increased lactate efflux from muscle, but it cannot be confirmed whether this represents an increased rate of glycolysis within the muscle.

Adult↗
PubMed2002

Effect of alkalosis on plasma epinephrine responses to high intensity cycle exercise in humans.

The purpose of this study was to determine the effects of alkalosis on epinephrine concentrations in response to a 90 s maximal exercise test. A group of ten healthy men ingested either a bicarbonate (BS) supplement (0.3 g x kg(-1) of body mass of sodium bicarbonate) or placebo mixture (P) prior to performing a 90 s maximal cycle ergometer test. An indwelling Teflon cannula was placed in the antecubital vein and blood samples were drawn at three times at rest separated by 10 min, immediately following the protocol, and at 2.5, 5, and 10 min post exercise to determine plasma epinephrine concentrations. Sodium bicarbonate ingestion significantly ( P<0.05) induced alkalosis both at rest [mean (SD) pH=7.42 (0.02) BS, 7.38 (0.02) P] and after the exercise protocol [pH=7.16 (0.02) BS, 7.12 (0.02) P]. Plasma epinephrine concentrations were not significantly different immediately post exercise between the two conditions [4.2 (0.6) compared to 4.2 (0.7) pmol x ml(-1) in BS and P, respectively]. Work performed and power output attained were not significantly different between the two treatment conditions [mean power=258.7 (35.1) W BS, 260.3 (35.4) W P; peak power=534.7 (61.6) W BS, 535.7 (54.4) W P]. The primary finding of this investigation was that orally-induced alkalosis does not significantly affect plasma epinephrine concentrations or performance following 90 s of maximal cycle exercise in untrained men.

Acid-Base Equilibrium↗
PubMed1983

Treatment of metabolic alkalosis with intravenous infusion of concentrated hydrochloric acid.

A concentrated hydrochloric acid (1 N) infusion was utilized for treatment on 35 occasions of metabolic alkalosis in 24 patients. The amount of hydrochloric acid to be infused was calculated from total base excess. To avoid over-correction, two thirds of the calculated dosage of hydrochloric acid only was infused. 1 N hydrochloric acid solution was infused at a speed of 1 mEq/min through a roentgenographically confirmed central venous line. Metabolic alkalosis was successfully treated in all instances without any complication. However, increased respiratory stimulation was not demonstrated in these observations. Concentrated hydrochloric acid infusion is a safe, reliable, and effective method of rapid correction of metabolic alkalosis. Because only small volumes are needed, this method is especially useful when fluid intake must be restricted.

Adult↗
PubMed1978

Severe hypercapnia associated with a non-respiratory alkalosis.

A case of hypoventilation in response to a non-respiratory alkalosis is presented. It is postulated that the degree of hypoventilation encountered was a normal response and that a fall in intracellular hydrogen ion concentration was responsible for the hypoventilation. This explains why the alkalosis associated with potassium deficiency is not associated with hypoventilation since the intracellular hydrogen ion concentration then remains constant. The renal response in this condition is responsible for maintaining the alkalosis and seems to be aimed at sodium conservation and hence plasma volume control rather than defence of acid-base balance.

Alkalosis↗
PubMed1977

Hypoglycemia induced by alpha-adrenergic stimulation during alkalosis.

Hypoglycemia developed during respiratory alkalosis in fasted rats. This hypoglycemia was markedly potentiated by the simultaneous injection of inhibitors of hepatic gluconeogenesis or a beta-adrenergic blocking agent; was not influenced by anti-insulin serum; was attenuated by hexamethonium; and was abolished by an alpha-adrenergic blocking agent. The rate of removal of injected glucose by peripheral tissues increased during alkalosis in insulin-deficient rats. The uptake of [14C]-glucose by the adipose tissue in vivo, which is stimulated by a very minute amount of insulin, was also stimulated during alkalosis whether or not the circulating insulin was neutralized with anti-insulin serum. It was concluded that, in alkalotic rats, blood glucose is rapidly utilized by peripheral tissues dependent on alpha-adrenergic stimulation, but without mediation of insulin and that this leads to development of hypoglycemia.

Alkalosis, Respiratory↗
PubMed1984

Ventilatory adaptation to metabolic alkalosis in adult awake potassium restricted rats.

The resting ventilation of awake rats, developing metabolic alkalosis as a result of sustained dietary potassium (K) restriction, was compared to that of age-matched controls. Extending the measurements over 17 weeks and using adult rats indicated, as soon as the third week, a significant progressive fall in the minute ventilation of low K rats, which previous studies limited to a single time determination did not consistently ascertain. The ventilatory adaptation observed in all groups, as well as the superimposed respiratory compensation to metabolic alkalosis in low K rats, resulted only from frequency changes. In both groups, the duration of inspiration was inversely correlated with the age of the animals. The duration of expiration was stable in controls but increased significantly with time in low K rats. According to these data, the respiratory compensation to K-depletion alkalosis in the rat is achieved only through an adjustment in the timing component of the control of breathing.

Alkalosis↗
PubMed1997

The effect of metabolic acidosis and alkalosis on the H+-ATPase of rat cerebral microvessels.

To determine the role of the proton translocating adenosine triphosphatase (H+-ATPase) of the blood-brain barrier, the density of the 31 Kd subunit of the vacuolar type H+-ATPase was quantitated in isolated rat cerebral microvessels with immunoblotting techniques. To establish the tissue specificity of the findings, synaptosomal membranes were also studied. Metabolic acidosis was induced with 1.5% ammonium chloride in drinking water for five days. Metabolic alkalosis was induced with 2.35% NaHCO3 in drinking water and daily injections of 10 mg/Kg furosemide intraperitoneally for 5 days. The quantity of the 31 Kd subunit (in arbitrary units) in cerebral microvessels was significantly increased in acidosis (3.98 +/- 0.45) (p<0.05) and was significantly decreased in metabolic alkalosis (0.49 +/- 0.16) (p<0.00) compared to controls (1.77 +/- 0.73). In synaptosomal membranes, metabolic alkalosis was associated with significant decrease in the quantity of the 31 Kd subunit-H+-ATPase (0.62 +/- 0.12 vs 0.92 +/- 0.01) p<0.05. The increase in the 31 Kd subunit in synaptosomal membranes with acidosis did not reach statistical significance. It is concluded that the quantity of vacuolar H+-ATPase in the blood-brain barrier is modulated by blood H+ or HCO3- content. These changes may be relevant to the physiology of the acid-base balance in the central nervous system.

Acidosis↗
PubMed2001

Hypokalemia, metabolic alkalosis, and hypertension: Cushing's syndrome in a patient with metastatic prostate adenocarcinoma.

Ectopic adrenocorticotropic hormone (ACTH) and/or corticotropin-releasing hormone (CRH) are associated with a growing list of tumors. We report a 69-year-old white man with a history of high-grade prostate carcinoma and widely metastatic adenocarcinoma who presented with metabolic alkalosis, hypokalemia, and hypertension secondary to ectopic ACTH and CRH secretion. Laboratory values were consistent with hypokalemia and metabolic alkalosis. Markedly elevated serum cortisol (135 microg/dL), ACTH (1,387 pg/dL), CRH (69 pg/dL), and urine free cortisol (16,276 microg/24 h) levels were found. Chest computed tomographic (CT) scan showed small noncalcified parenchymal densities; however, bronchoscopy and bronchoalveolar lavage washings were unremarkable for a neoplastic process. Abdominal CT scan and magnetic resonance imaging showed multiple small liver lesions and multiple thoracic and lumbar intensities consistent with diffuse metastatic disease. Histological analysis of a biopsy specimen from the thoracic spine showed an undifferentiated adenocarcinoma consistent with a prostate primary tumor. The severe metabolic alkalosis secondary to glucocorticoid-induced excessive mineralocorticoid activity was treated with potassium supplements, spironolactone, and ketoconazole. In this case report, we describe an unusual tumor associated with ectopic ACTH and CRH production and the pharmacodynamic relationship of plasma cortisol levels and urinary cortisol excretion with ketoconazole treatment.

ACTH Syndrome, Ectopic↗
PubMed2000

Reversal of hypercapnia induces KATP channel and NO-independent constriction of basilar artery in rabbits with acute metabolic alkalosis.

The mechanism of hypocapnic constriction of the cerebral vasculature under conditions of altered acid-base balance has not been investigated. As K(ATP) channels and NO have been implicated in hypocapnic constriction, this study investigated their roles in the constriction due to lowered pCO(2) in hypercapnic rabbits with acute metabolic alkalosis. Metabolic alkalosis was induced acutely following ketamine/xylazine injection. Lowering blood pCO(2) from initial baseline hypercapnic levels to near normocapnic and hypocapnic levels constricted basilar artery by 10.2+/-0.8% (4) and 16.2+/-0.6% (44), respectively (means+/-S.E., n), as determined in an in situ cranial window preparation. The constrictions were maintained for 4-5 h and return of pCO(2) to hypercapnic levels relaxed the constriction. Changing the suffusate pH to either the pH of the cerebral spinal fluid observed during initial baseline hypercapnia or following lowered pCO(2) did not alter the magnitude of constriction due to lowered pCO(2). Neither 0.3 mM N(G)-monomethyl-L-arginine monoacetate, an NO synthase inhibitor, nor 10 microM glibenclamide, a K(ATP) channel blocker, altered the magnitude of hypocapnic constriction. These results demonstrated that under conditions of acute metabolic alkalosis and accompanying compensatory hypercapnia, subsequent pCO(2) reduction induces prolonged constriction of the basilar artery that is independent of (1) cerebral spinal fluid pH over a physiologic range, and (2) NO and K(ATP) channels.

ATP-Binding Cassette Transporters↗
PubMed2000

Reversal of hypercapnia induces endothelin-dependent constriction of basilar artery in rabbits with acute metabolic alkalosis.

We recently concluded that constriction of basilar artery due to respiration-induced hypocapnia in rabbits with acute metabolic alkalosis and accompanying compensatory hypercapnia was independent of NO and K(ATP) channels. Based on reports that endothelin-1-mediated hypocapnic constriction of the rabbit basilar artery in vitro, we further investigated whether the respiration-induced hypocapnic constriction was endothelin-1 mediated. Metabolic alkalosis was induced acutely following ketamine/xylazine injection. The ET(A) plus ET(B) receptor antagonist, PD145065 (1 microM), and the selective ET(A) receptor antagonist, BQ610 (3 microM), completely relaxed the hypocapnic constriction, as determined in a cranial window. Unexpectedly, the ET(B) receptor antagonists, BQ788 and RES-701-1 (3 microM), relaxed the constriction by 72.1+/-2.8% (4) and 77.2+/-8.7% (5), respectively (means+/-S.E. (n)). To investigate whether the large magnitudes of relaxation to both ET(A) and ET(B) receptor antagonists were due to nonselectivity of the antagonists, the effects of the antagonists on the constriction to exogenous endothelin-1 were evaluated. BQ610, BQ788, and RES-701-1 relaxed the 3-5 nM endothelin-1 constriction by only 64.3+/-7.6% (4), 43.5+/-8.5% (5), and 26.7+/-4.8% (3) (means+/-S.E. (n)), respectively, consistent with the selective blocking action of these antagonists. To investigate whether the greater magnitude of BQ610, BQ788, and RES-701-1 relaxation of hypocapnic constricted versus exogenous endothelin-1-constricted vessels was due to differences between constriction elicited by endogenous versus exogenous endothelin-1, the effects of the endothelin receptor antagonists on constriction to isocapnic alkaline suffusate were evaluated. PD145065 (1 microM) and 0.1 mM phosphoramidon, an endothelin-converting enzyme inhibitor, inhibited the constriction to isocapnic alkaline suffusate by 83.8+/-7.8% (6) and 74.3+/-9.7% (8) (means+/-S.E. (n)), respectively, consistent with the endothelin-1 dependency of the constriction. BQ610, BQ788, and RES-701-1 relaxed the isocapnic alkaline suffusate constriction by 74.9+/-6.7% (5), 65.5+/-6.4% (5), and 78.0+/-6.5% (4) (means+/-S.E. (n)), respectively. Thus, the relaxation profile to the selective endothelin receptor antagonists in isocapnic alkaline constricted vessels more closely approximated the relaxation profile observed in hypocapnic constricted as compared to endothelin-1-constricted vessels. Hypocapnia did not alter the 5 nM endothelin-1 constriction. These results suggest that, under conditions of acute metabolic alkalosis and accompanying compensatory hypercapnia, subsequent hypocapnic constriction is endothelin mediated. Both ET(A) and ET(B) receptor activation may mediate the hypocapnic constriction. The hypocapnic constriction is not due to enhanced endothelin-1 constriction and, thus, is due to the release of endothelin-1 and/or additional endothelins.

Alkalosis↗
PubMedDate not supplied

Severe metabolic alkalosis due to baking soda ingestion: case reports of two patients with unsuspected antacid overdose.

Oral ingestion of baking soda (sodium bicarbonate) has been used for decades as a home remedy for acid indigestion. Excessive bicarbonate ingestion places patients at risk for a variety of metabolic derangements including metabolic alkalosis, hypokalemia, hypernatremia, and even hypoxia. The clinical presentation is highly variable but can include seizures, dysrhythmias, and cardiopulmonary arrest. We present two cases of severe metabolic alkalosis in patients with unsuspected antacid overdose. The presentation and pathophysiology of antacid-related metabolic alkalosis is reviewed.

Adult↗
PubMed1990

Time course of postischemic intracellular alkalosis reflects the duration of ischemia.

We investigated the long-term (up to 1 week) relationships between the duration of cerebral ischemia and postischemic energy metabolic profile, pH, and tissue edema in the rat. Ten rats each were subjected to 8 or 12 min of forebrain ischemia induced by bicarotid occlusion concurrent with systemic hypotension, and the results were compared with those of 10 sham-operated rat controls. In vivo 31P nuclear magnetic resonance spectroscopy was performed prior to ischemia and at intervals up to 168 h after ischemia. Cerebral edema (measured by specific gravity) was assessed prior to ischemia and at 24, 72, and 168 h after ischemia. The data revealed significant differences in the brain tissue pH profile over time between the ischemic groups (p less than 0.03). The 12-min ischemic animals exhibited brain tissue alkalosis (pH = 7.27 +/- 0.12) at 24 h compared with both sham (pH = 7.09 +/- 0.08) at 24 h and preischemic (pH = 7.06 +/- 0.04) pH values. The pH remained alkalotic (pH = 7.23 +/- 0.15) through the 48-h time period. In contrast, in the 8-min group, the onset of alkalosis was delayed until 48 h after ischemia (pH = 7.24 +/- 0.15), and pH remained alkalotic for only 24 h. No difference in high-energy phosphate metabolism was detected between groups. A different time dependence of tissue pH and specific gravity changes after 12 min of ischemia was detected. The present study suggests that the duration of an ischemic event marks the time of onset of brain tissue alkalosis and its duration and that cerebral edema alone cannot explain the pH changes.

Alkalosis↗
PubMed1979

Effects of metabolic acidosis and alkalosis on sodium and calcium transport in the dog kidney.

Clearance and micropuncture studies have been performed in dogs to examine the effects of acute and chronic metabolic acidosis and acute alkalosis on tubular sodium and calcium transport. Acute metabolic acidosis, induced by the infusion of hydrochloric acid, decreased proximal fluid reabsorption and increased the fractional delivery of sodium and calcium to the distal tubule, but not to the final urine. In comparison with normal dogs, dogs with chronic metabolic acidosis (induced by feeding ammonium chloride) showed an increase in proximal fluid reabsorption and a dissociation of calcium from sodium reabsorption more distally, leading to an increased delivery of calcium relative to sodium at the distal tubule and in the final urine. The infusion of sodium bicarbonate to correct chronic metabolic acidosis, both in intact and thyroparathyroidectomized (TPTX) dogs, reduced proximal fluid reabsorption and caused a selective enhancement of calcium reabsorption relative to sodium in the more distal nephron, resulting in a reversal of the dissociation observed in acidosis, both at the distal tubule and in the final urine. By contrastin fusion of sodium chloride in parathyroid-intact acidotic dogs did not reduce proximal fluid reabsorption or enhance tubular calcium reabsorption. In nonacidotic dogs, both intact and TPTX, infusion of sodium bicarconate to induce acute alkalosis resulted in selhese data demonstrate the presence of a component of tubular calcium reabsorption situated beyond the proximal tubule, which is inhibited by chronic (but not acute) metabolic acidosis and enhanced by metabolic alkalosis (or bicarbonate infusion) independently of parathyroid hormone.

Acidosis↗
PubMed1984

Reduced glomerular filtration and enhanced bicarbonate reabsorption maintain metabolic alkalosis in humans.

The mechanism that sustains chloride-depletion metabolic alkalosis is presumed to be a stimulation of renal acidification, so that the elevated filtered bicarbonate load that attends hyperbicarbonatemia is completely reabsorbed. However, such enhancement of renal bicarbonate reabsorption is not necessary to maintain hyperbicarbonatemia if the filtered bicarbonate load is not increased owing to a concomitant reduction in glomerular filtration rate (GFR). To assess the relative contributions of enhanced renal bicarbonate reabsorption and reduced GFR in the maintenance of chloride-depletion alkalosis in humans, selective hydrochloric acid depletion was induced in five normal subjects. Plasma bicarbonate concentration increased by 27% (25.3 +/- 0.1 to 32.1 +/- 0.3 mEq/liter, P less than 0.005), whereas the rate of renal bicarbonate reabsorption increased by only 17% (2.7 +/- 0.1 to 3.2 +/- 0.2 mEq/min, P less than 0.05) owing to a 10% reduction in GFR (93.2 +/- 4.4 to 84.3 +/- 4.1 ml/min, P less than 0.01). Thus, in chloride-depletion metabolic alkalosis in humans, the increase in plasma bicarbonate concentration is not attended by a commensurate increase in filtered bicarbonate and rate of renal bicarbonate reabsorption. Both a reduction in GFR and an enhancement of renal bicarbonate reabsorption contribute to maintenance of the alkalotic state.

Absorption↗
PubMed1987

Renal response to metabolic alkalosis induced by isovolemic hemofiltration in the dog.

We describe a new model of chloride-depletion alkalosis (CDMA), in which the method of induction of alkalosis does not itself cause a direct alteration in sodium and fluid balance. We have used this model, which is based on hemofiltration techniques in the dog, to study the immediate response of the kidney to the induction of CDMA. Normal dogs maintained with a NaCl-free diet for several days underwent hemofiltration of 50 ml/kg over a 35 minute period. The hemofiltrate was replaced ml for ml with a solution containing sodium and potassium in the same concentrations as found in each animal's plasma water. In control animals, the replacement solution contained chloride and bicarbonate in the same ratio as in the plasma; in the experimental (CDMA) animals the replacement solution contained bicarbonate as the only anion. In the control group, the procedure of hemofiltration coupled with isovolemic replacement caused no appreciable changes in plasma composition, urinary excretion rates, GFR, or tubular handling of bicarbonate. In the CDMA group, 106 +/- 8.4 mEq of chloride were removed in exchange for bicarbonate. A marked metabolic alkalosis resulted, plasma bicarbonate concentration increasing from 21.9 +/- 0.6 to 33.3 +/- 0.6 mEq/liter. The hemofiltration procedure itself, by design, did not alter sodium or fluid balance. Nevertheless, cumulative urinary sodium excretion increased over 2.5 hours by 23.0 +/- 6.4 mEq. A natriuresis of this magnitude is equivalent to a loss of ECF volume of approximately 200 ml. GFR did not change significantly. The rate of tubular reabsorption of bicarbonate increased significantly from 1209 +/- 82 to 1559 +/- 148 mu Eq/min in CDMA animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalosis↗