Effect of Adrenalectomy on Production and Excretion of Ammonia by the Kidneys

1957 ◽  
Vol 188 (3) ◽  
pp. 524-528 ◽  
Author(s):  
Jean D. Wilson ◽  
Donald W. Seldin

The rate and magnitude of ammonia excretion and renal glutaminase adaptation is normal in adrenalectomized rats given moderate (up to 4 mEq/day) amounts of NH4Cl. The administration of large amounts of NH4Cl (5 mEq/day or more) invariably kills adrenalectomized rats. Shortly before death, renal glutaminase adaptation was normal. Survival of adrenalectomized rats on large amounts of NH4Cl could be prolonged if potassium was eliminated from the diet. Notwithstanding the prevention of hyperkalemia by restricting potassium intake and salt depletion by the provision of adequate amounts of sodium chloride, ammonia excretion is impaired in rats given large doses of NH4Cl despite normal adaptation of renal glutaminase. It is suggested that adrenal steroids are not involved in either the maintenance or activation of the glutaminase enzyme system in the kidneys of rats. In adrenalectomized rats given large doses of NH4Cl, the diminished excretion of ammonia appears to be a consequence of a diminished Na+–H+ exchange resulting from two disturbances: a) reduced delivery of Na+ to distal tubular exchange site, owing to peripheral circulatory insufficiency arising from salt depletion or potassium intoxication; b) a specific impairment of tubular reabsorption of Na+ owing to the absence of adrenal steroids.

1986 ◽  
Vol 250 (5) ◽  
pp. F930-F941 ◽  
Author(s):  
L. Rabinowitz ◽  
C. J. Wydner ◽  
K. M. Smith ◽  
H. Yamauchi

Diurnal potassium cycles (DPC) were measured in unanesthetized undisturbed rats fed a liquid diet and maintained in a 12-h light-dark environment. A fourfold step increase in diet potassium content increased DPC amplitude without altering phase. After presentation of the high-potassium diet, the initial adaptive increase in excretion occurred within 1.5 h (diet given during dark phase) and within 6 h (diet given during light phase). On a day when food was withheld (no potassium intake), DPC were present but with a lowered amplitude. The amount of potassium excreted on a fasting day exceeded gut and extracellular fluid potassium content and was only modestly increased when rats were previously fed a high-potassium diet. In adrenalectomized rats that received no steroid replacement or received constant infusions of low levels of aldosterone, dexamethasone, or aldosterone plus dexamethasone, potassium balance and DPC were normal. It is concluded that the amplitude of DPC in the rat is determined in part by the availability of potassium from both intracellular and extracellular potassium pools; mechanisms independent of potassium intake can generate the DPC; and the presence or the cyclic secretion of adrenal steroids is not necessary for the generation of DPC in the rat.


1973 ◽  
Vol 19 (11) ◽  
pp. 1243-1247 ◽  
Author(s):  
P A Drinker ◽  
D C Noonan ◽  
N Ramanaiah ◽  
J R Tole

Abstract Two different blood-gas analyzers were tested to determine the effects on blood pH measurement of changing the reference bridge solution from saturated KCl to normal saline (0.16 mol of NaCl per liter). This change, which necessitated the preparation of modified buffers equimolal in NaCl with respect to blood, virtually eliminated salt depletion of the bridge solution and improved the stability of the liquid-junction potential between the bridge solution and the sample. The instruments we used were the Corning 165 pH Blood Gas Analyzer and the Radiometer E5021 pH Electrode with PHM72 Acid Base Analyzer. Comparison of results on clinical blood samples indicates that performance with the modified bufferbridge system is the same as that obtained with the conventional scheme. Analytical performances of the Corning and Radiometer instruments for PO2 and PCO2, as well as for pH, were comparable.


1958 ◽  
Vol 195 (1) ◽  
pp. 142-146 ◽  
Author(s):  
Joseph H. Perlmutt ◽  
Donald A. Olewine

The increased urinary Na+ output induced by Diamox in water-loaded adrenalectomized rats was partially antagonized by the mineralocorticoid, desoxycorticosterone glucoside (DCG), the increased K+ excretion was augmented and urine volume was not affected. Intact rats subjected to the same treatment showed only a small, but significant, rise in K+ excretion. Under the same conditions, the glucocorticoid, hydrocortisone hemisuccinate (compound FH), significantly elevated Na+, K+ and H2O excretion in adrenalectomized rats receiving Diamox; intact rats showed an increase in Na+ and H2O excretion with no significant change in K+ output. Of particular interest is the finding that 2.5 mg compound FH alone increased H2O excretion in adrenalectomized rats to a slightly greater extent than Diamox alone with considerably less Na+ loss.


1985 ◽  
Vol 249 (4) ◽  
pp. F596-F602
Author(s):  
W. J. Welch ◽  
C. E. Ott ◽  
G. P. Guthrie ◽  
T. A. Kotchen

Renin release is increased in the adrenalectomized rat and is not inhibited by sodium chloride administration. The purpose of this study was to determine whether increased renin release is related to impaired absorptive chloride transport in the loop of Henle. Chloride transport in the loop was measured before and after acute saline infusion in three groups of rats: 1) saline-drinking adrenalectomized rats (Adx); 2) saline-drinking dexamethasone-treated adrenalectomized rats (Dex); and 3) water-drinking sham-operated controls. Unrelated to differences of arterial pressure, glomerular filtration rate, or net sodium chloride balance, chloride reabsorption in the loop of Henle of Adx [836 +/- 172 peq/min (SE)] was less (P less than 0.01) than in controls (1,646 +/- 353) and Dex (1,377 +/- 318) before saline infusion. After saline infusion, chloride delivery to the loop increased (P less than 0.05) in all three groups. However, loop chloride reabsorption increased (P less than 0.01) only in controls and Dex but not in Adx. Before saline infusion, plasma renin concentration (PRC) of Adx (350 +/- 108 U/ml) was greater (P less than 0.01) than that in controls (56 +/- 6) or Dex (108 +/- 36); sodium chloride infusion failed to inhibit PRC in Adx, whereas PRC was suppressed (P less than 0.01) by saline in Dex and controls. Thus stimulation of renin release in adrenalectomized animals was associated with decreased absorptive chloride transport in the loop of Henle. Dexamethasone normalized loop function and renin responsiveness to sodium chloride.


1965 ◽  
Vol 208 (6) ◽  
pp. 1281-1285 ◽  
Author(s):  
George Wolf

The effect of DOC on sodium chloride (saline) intake was studied in intact and adrenalectomized rats under "two-bottle" self-selection conditions. It was found that in adrenalectomized rats low doses of DOC produced a decrease in saline intake (restoration of sodium-retaining ability), whereas high doses produced an increase in saline intake (stimulation of sodium appetite). At high doses, however, intact rats consumed more saline and manifested a greater preference for it than did similarly treated adrenalectomized rats. Treatment with corticosterone increased both absolute saline intake and saline preference of DOC-treated adrenalectomized rats.


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