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The defense of brain volume during hyponatremia cannot be explained by the losses of brain sodium and potassium. We have examined the brain losses of organic osmolytes in rats after 24 h of severe hyponatremia induced by the administration of vasopressin and 5% dextrose in water. Normonatremic controls and animals with intermediate plasma sodium concentration ([Na]) were produced in vasopressin-treated animals by the administration of isocaloric gavages containing varying amounts of NaCl and free water. The animals were killed at 24 h by decapitation, and one brain hemisphere was quickly frozen in liquid nitrogen for organic osmolyte determinations. When compared with controls (plasma [Na] = 139 +/- 1.5 mM), hyponatremic animals (plasma [Na] = 96 +/- 1 mM) had significantly reduced brain contents for sodium, potassium, chloride, glutamate, myo-inositol, N-acetylaspartate, aspartate, creatine, taurine, gamma-aminobutyric acid, and phosphoethanolamine. Plasma [Na] was highly correlated (P < 0.001) with the brain contents for sodium, potassium, and organic osmolytes. Whereas the observed increase in brain water during hyponatremia was only 4.8%, by calculation, brain swelling without brain organic osmolyte losses would have been 11%, an amount that jeopardizes survival.

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Studies were performed to evaluate the contribution of the urea appearance rate to the elevated plasma urea concentration found during diuretic-induced sodium depletion. Negative sodium balance of -1162 + 29 microEq/100 g body wt was induced over a four day period by the administration of furosemide, 20 to 30 mg/kg/d i.p., to rats ingesting a sodium free diet. When compared with sodium replete controls, sodium depletion significantly increased the plasma urea concentration (65.0 +/- 3.1 vs. 26.4 +/- 1.1 mg/dl) through both an increase in the urea appearance rate (160 +/- 5.2 vs. 125 +/- 3.5 mg/day/100 g body wt), and a decrease in the urea clearance rate (1.99 +/- 0.14 vs. 3.16 +/- 0.12 ml/min/kg). The urea appearance rate increased on the first day of diuretic administration, remained elevated three days after stopping diuretics, rapidly returned to control levels after sodium repletion, and was significantly correlated with the magnitude of sodium deficit. Similar results were obtained when diuretic-induced sodium depletion was produced in adrenalectomized animals. After four days of sodium depletion the plasma concentration was increased for some amino acids but not for the plasma total amino acid, nitrogen concentration. The results indicate that sodium depletion increases the urea appearance rate through a mechanism that is independent of adrenal function. Thirty to sixty percent of the elevation in plasma urea concentration that occurs in the rat during diuretic-induced sodium depletion can be accounted for by an enhanced urea appearance rate.

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By abolishing the large splanchnic uptake of amino acids, evisceration-hepatectomy unmasks the tendency for peripheral tissues to release increased amounts of amino acids into the extracellular fluid during sodium depletion. The increase in amino acid delivery to the liver may stimulate hepatic urea synthesis both by providing more substrates for conversion to urea and perhaps also by stimulation of the activity of urea cycle enzymes.

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Hypertension secondary to hydronephrosis is uncommon, and when a duplex system is involved it is rare. A patient presenting with hypertension and an abdominal mass on the left side was found to have a non-functioning, massively dilated upper pole of a duplex system causing hyperreninemic hypertension. Treatment consisted of an upper pole partial nephrectomy. This unique case is discussed and the literature regarding hypertension secondary to hydronephrosis is reviewed.

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Selective renal artery catheterization and renal angiography are commonly performed diagnostic procedures; however, the effects of these procedures on renal blood flow (RBF) and renin release have only been partially described. A biphasic RBF response has been well documented furing selective angiography in dogs. The renal autoregulatory mechanisms governing the responses are uncertain. The renin-angiotensin system and the major parameters of contrast media, hypertonicity and viscosity, have been suggested as important factors. In the canine model, we examined the acute changes in renal venous renin activity along with the renal hemodynamic effects of hypertonicity and viscosity. Our results do not support a primary effect mediated by the renin-angiotensin system. Hypertonicity and the contrast medium per se are significant in active and passive autoregulatory responses at the smooth muscle cellular level.

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Studies of the metabolism of glutamine and glutamate by renal cortex slices from acidotic, alkalotic, and control rats were performed. 88-95% of the glutamine and 104-115% of the glutamate taken up from the medium could be accounted for by the products found. Acidosis increased glutamine uptake and conversion to ammonia, CO(2), glucose, lactate, pyruvate, lipid, and protein. The increase in glutamine conversion to ammonia after acidosis could be completely accounted for by the associated increase in its conversion to glucose, glutamate, lactate, and pyruvate. When glutamate metabolism was examined, acidosis did not affect substrate uptake but did increase its conversion to ammonia, glucose, lactate, CO(2), and lipid. The increase in (14)CO(2) from U-(14)C-glutamine and U-(14)C-glutamate found with cortex slices from acidotic animals could be explained by the CO(2) production calculated to be associated with the enhanced conversion of these substrates to other products during acidosis. (14)CO(2) production from 1.2-(14)C-acetate was found to be significantly increased in alkalosis rather than acidosis. These studies suggest that in the rat, the rate at which glutamine is completely oxidized in the Krebs cycle is not a factor regulating renal ammonia production. A comparison of the effects of acidbase status on glutamine and glutamate metabolism suggests that either glutamine transport or glutamine transaminase activity are significantly increased by acidosis.

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In previous studies it was found that renal cortical slices from rats with induced metabolic acidosis have an increased capacity to produce glucose, whereas cortical slices from rats with metabolic alkalosis manifest decreased gluconeogenesis. To evaluate the relative influence of extracellular fluid pH, [HCO(3) (-)], and carbon dioxide tension on renal gluconeogenesis, we observed glucose production by cortex from rats with induced respiratory acidosis, and by cortex taken from normal animals and incubated in acid and alkaline media. We found glucose production to be increased in cortex from rats with respiratory acidosis, as is the case in metabolic acidosis. Glucose production by slices from normal rats was increased in media made acidic by reducing [HCO(3) (-)], and decreased in media made alkaline by raising [HCO(3) (-)]. These effects were evident whether the gluconeogenic substrate employed was glutamine, glutamate, alpha-ketoglutarate, or oxalacetate. Glucose production was also increased in media made acidic by raising CO(2) tension and decreased in media made alkaline by reducing CO(2) tension. These data indicate that both in vivo and in vitro, pH, rather than CO(2) tension or [HCO(3) (-)], is the most important acid-base variable affecting renal gluconeogenesis. The findings suggest that a decrease in extracellular fluid pH enhances renal gluconeogenesis through direct stimulation of one of the rate-limiting reactions involved in the conversion of oxalacetate to glucose. We hypothesize that the resultant increase in the rate of removal of glutamate, a precursor of oxalacetate, may constitute an important step in the mechanism by which acidosis increases renal ammonia production.

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