Reduction of Urea Generation and Muscle Protein Degradation by Adrenalectomy in Acutely Uremic Rats

Schaefer, Roland M.; Weipert, J.; Möser, Michael; Peter, G.; Heidbreder, E.; Hörl, Walter H.; Heidland, A.

doi:10.1159/000184895

Cited by 14 publications

(7 citation statements)

References 18 publications

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“…Studies in our laboratory have provided support to this notion. Following adrenalectomy, we observed reduced rates of urea nitrogen (urea-N) appear ance and a decrease of muscle protein breakdown in acutely uremic rats [16]. However, investigations em ploying adrenalectomy as a model of glucocorticoid defi ciency are always burdened by the fact that concomi tantly a considerable source of catecholamines is re moved from the organism.…”

Section: Introductionmentioning

confidence: 92%

Evidence for Reduced Catabolism by the Antiglucocorticoid RU 38486 in Acutely Uremic Rats

Schaefer¹,

Teschner²,

Kulzer³

et al. 1987

Am J Nephrol

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Previous studies suggested that increased blood levels of, or increased tissue sensitivity to, glucocorticoids may contribute to catabolism in acute uremia. To examine this possibility we determined urea nitrogen (urea-N) appearance, plasma levels of N^l-methylhistidine and the activity of the alkaline myofibrillar proteinase in acutely uremic rats with and without treatment with RU 38486, a selective antiglucocorticoid. Forty-eight hours after bilateral nephrectomy, the rats had markedly elevated serum levels of urea-N, creatinine, potassium and phosphorus. In uremic rats receiving RU 38486, comparable levels of serum creatinine were found, but the serum levels of urea-N (221 ± 4 vs. 259 ± 5 mg/dl) and phosphorus (6.5 ± 0.3 vs. 8.5 ± 0.4 mmol/l) were significantly decreased as compared to uremic animals without RU 38486. In comparison to sham-operated rats, urea-N appearance (net urea production) was increased by 56% 48 h after bilateral nephrectomy. This increment was almost completely reversed in uremic animals receiving the antiglucocorticoid. In untreated uremic rats, plasma levels of N_tethylhistidine were 10.3 ± 0.9 μg/dl, whereas the administration of RU 38486 caused a significant decline in the levels of this amino acid (7.6 ± 0.5 μg/dl). This reduction in N’-methylhistidine was associated with a concomitant decrease of myofibrillar proteinase activity in muscle tissue homogenates. Compared to sham-operated animals, this proteinase activity was increased by 30% in uremic rats, but was normal in those given RU 38486. Taken together, these data support the view that in acute uremia accelerated ureagenesis occurs, while enhanced muscle protein breakdown, owing to an increment in myofibrillar proteinase activity, provides the necessary amino acid precursors. Furthermore, the activity of this proteinase, and therefore the rate of muscle protein breakdown, strongly depend on the presence or absence of glucocorticoids in uremia.

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Section: Introductionmentioning

confidence: 92%

Evidence for Reduced Catabolism by the Antiglucocorticoid RU 38486 in Acutely Uremic Rats

Schaefer¹,

Teschner²,

Kulzer³

et al. 1987

Am J Nephrol

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“…Serum levels of BUN and creatinine and superoxide scavenging activity were used as indicators of renal protection. As one might suspect, an increase in the serum BUN level may also be induced by muscle protein breakdown [10,21], but muscle protein breakdown could not lead to an increase in the creatinine level [15]. As many authors have reported that an increase in both serum BUN and creatinine levels could be used clinically to imply renal insufficiency [5,20], we decided to choose the tests of serum BUN and creatinine levels as the indication of renal damage.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Tetramethylpyrazine on Absolute Ethanol-Induced Renal Toxicity in Mice

Liu

Lin

et al. 2002

J Biomed Sci

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Acute administration of absolute ethanol (10 ml/kg) per os to fasted mice produced extensive renal failure as measured by a rise in blood urea nitrogen and creatinine. Pretreatment with oral administration of tetramethylpyrazine (TMP) prevented such failure. The maximal effect against absolute ethanol-induced renal failure could be observed 1 h after TMP administration. In order to further investigate the renal protective mechanism of TMP, experiments on lipid peroxidation and superoxide scavenging activity were conducted. Renal homogenates made from mice treated with ethanol showed that TMP pretreatment had an antioxidant effect. Mice in acute renal failure had higher malonic dialdehyde concentrations than those pretreated with TMP. The renal protective mechanism of TMP was attributed, in part, to its prominent superoxide scavenging effect, which protects the kidney from superoxide-induced renal damage.

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“…After indomethacin application these parameters were within the same range in both BN groups as compared to sham animals. Furthermore, the UNA, which indicates protein degradation and provides us with information on the amount of amino acid release from skeletal muscle [3,9,16], was calculated for 48 h. The UNA significantly increased in both BN groups as compared to sham animals but did not change significantly with indomethacin treatment. The amino acid N~-MH has been found to be a parameter of myofibrillar breakdown since it is present solely within actin and myosin, and once it is released from skeletal muscle it cannot be reutilized [4,6,18].…”

Section: Discussionmentioning

confidence: 99%

“…As an indicator of protein degradation the urea nitrogen appearance (UNA) for 48 h was calculated [3,9]. Furthermore N~-methylhistidine (N~-MH) serum concentration was assayed [4,16] to estimate myofibrillar breakdown and also routine laboratory parameters (serum urea nitrogen, SUN; creatinine, potassium) were followed.…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin synthetase inhibitors are not beneficial in the hypercatabolic state of acute uremia in rats

1988

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In rats the effect of prostaglandin synthetase inhibition on the enhanced protein degradation in acute uremia was investigated. After 48 h of bilateral nephrectomy the urea nitrogen appearance, an indicator of net protein degradation, was calculated, and N tau-methylhistidine (N tau-MH) serum concentration was measured for judging myofibrillar breakdown. Also serum urea nitrogen, creatinine, and potassium serum concentrations were followed up. All bilateral nephrectomized rats showed severe uremic disturbances with increased (P less than 0.01) concentrations of serum urea nitrogen, creatinine, and potassium. Moreover, the urea nitrogen appearance and N tau-MH serum concentration increased (P less than 0.05) significantly. Administration of indomethacin (4 mg.kg-1b.wt./12 hi.p.) in bilateral nephrectomized rats did not influence the analyzed parameters significantly. Thus, we could not demonstrate a positive influence on the increased skeletal muscle degradation in acutely uremic rats by prostaglandin synthetase inhibition. These data suggest that in our model of acute uremia prostaglandins do not play a major role in the degradation of striated muscle.

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Reduction of Urea Generation and Muscle Protein Degradation by Adrenalectomy in Acutely Uremic Rats

Cited by 14 publications

References 18 publications

Evidence for Reduced Catabolism by the Antiglucocorticoid RU 38486 in Acutely Uremic Rats

Evidence for Reduced Catabolism by the Antiglucocorticoid RU 38486 in Acutely Uremic Rats

Protective Effect of Tetramethylpyrazine on Absolute Ethanol-Induced Renal Toxicity in Mice

Prostaglandin synthetase inhibitors are not beneficial in the hypercatabolic state of acute uremia in rats

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