Effect of chronic renal failure on Na,K-ATPase alpha 1 and alpha 2 mRNA transcription in rat skeletal muscle.

Bonilla, Silvia; Goecke, I. Annelise; Bozzo, S.R.; Alvo, Miriam; Michea, Luis; Marusic, Elisa T.

doi:10.1172/jci115544

Cited by 29 publications

(21 citation statements)

References 28 publications

(19 reference statements)

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“…Somatostatin administration to fasting rats is followed by a greater increase in plasma potassium in uremic than in normal animals (48). Moreover, the ouabaininhibitable rubidium uptake by skeletal muscle from uremic rats is impaired (49). These observations in animals are in agreement with clinical studies, and show that fasting is followed by a rise in serum potassium in dialysis patients, but not in controls (50).…”

Section: Discussionsupporting

confidence: 63%

Effects of recombinant human growth hormone on muscle protein turnover in malnourished hemodialysis patients.

Garibotto¹,

Barreca²,

Russo³

et al. 1997

J. Clin. Invest.

106

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To assess the effect of recombinant human growth hormone (rhGH) on muscle protein metabolism in uremic patients with malnutrition, forearm [ 3 H]phenylalanine kinetics were evaluated in six chronically wasted (body weight 79% of ideal weight) hemodialysis (HD) patients in a self-controlled, crossover study. Forearm protein dynamics were evaluated before, after a 6-wk course of rhGH (5 mg thrice weekly) and after a 6-wk washout period. After rhGH: ( a ) forearm phenylalanine net balance-the difference between phenylalanine incorporation into and phenylalanine release from muscle proteins-decreased by 46% ( Ϫ 8 Ϯ 2 vs. Ϫ 15 Ϯ 2 nmol/min·100 ml at the baseline and Ϫ 11 Ϯ 2 after washout,

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Section: Discussionsupporting

confidence: 63%

Effects of recombinant human growth hormone on muscle protein turnover in malnourished hemodialysis patients.

Garibotto¹,

Barreca²,

Russo³

et al. 1997

J. Clin. Invest.

106

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“…Da Silva et al (37) found significant decreases in cardiac mRNA for ␣2 without any changes in ␣2 protein observed. Bonilla et al (38) reported decreases in both Na ϩ /K ϩ ATPase activity as well as mRNA for the ␣1 isoform in skeletal muscle; however, these workers found an increase in ␣2 mRNA in this tissue. At present, the reason(s) for the discrepancy between our findings and these other studies is/are not clear.…”

Section: Discussionmentioning

confidence: 91%

Effect of Chronic Renal Failure on Cardiac Contractile Function, Calcium Cycling, and Gene Expression of Proteins Important for Calcium Homeostasis in the Rat

Kennedy

Omran

Periyasamy

et al. 2003

Journal of the American Society of Nephrology

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Abstract. Patients with chronic renal failure frequently develop cardiac hypertrophy and diastolic dysfunction; however, the mechanisms by which this occurs are still unclear. Male Sprague-Dawley rats were subjected to 5/6 nephrectomy and studied for their isolated myocyte function, calcium cycling, and gene expression of proteins important in calcium homeostasis after 4 wk. Comparable rats subjected to suprarenal aortic banding for the same duration were used for comparison. Rats subjected to 5/6 nephrectomy and aortic banding developed comparable hypertension; however, rats subjected to 5/6 nephrectomy experienced a greater degree of cardiac hypertrophy and downregulation of cardiac sodium potassium ATPase (Na ϩ /K ϩ -ATPase) activity than rats subjected to aortic banding. Moreover, cells isolated from the 5/6 nephrectomy rat hearts displayed impaired contractile function and altered calcium cycling compared with cells isolated from control or aortic constriction rat hearts. The 5/6 nephrectomy rat heart cells displayed a prolonged time constant for calcium recovery following stimulation, which corresponded to decreases in homogenate sarcoplasmic reticulum calcium ATPase-2a (SERCA2a) activity, protein density, and mRNA for SERCA2a. In conclusion, chronic renal failure leads to alterations in cardiac gene expression, which produces alterations in cardiac calcium cycling and contractile function. These changes cannot be explained only by the observed increases in BP. jshapiro@mco.eduPatients with renal failure usually develop cardiac complications. In end-stage renal disease (ESRD) patients treated with hemodialysis in the United States, annual mortality rates exceed 20%, with more than 50% attributed to cardiac mortality (1). Although the term "uremic cardiomyopathy" had previously been used to refer to a dilated cardiomyopathy complicating renal failure, more recent studies suggest that the most common form of heart disease in renal failure patients is one characterized by diastolic dysfunction and left ventricular hypertrophy (2). Although a number of known factors have been implicated in the pathogenesis of the left ventricular hypertrophy and diastolic dysfunction, our understanding of these processes is still incomplete (3).For many years, it has been known that the sodium pump is abnormal in chronic renal failure and that circulating inhibitor(s) can be demonstrated in the serum of uremic patients (4 -6). We have observed that sodium pump inhibition initiates a signal cascade that can cause alterations in gene transcription and ultimately produce hypertrophy in cardiomyocytes grown in culture (7-9). We have also observed that sodium pump inhibitors, including those circulating in the serum of uremic patients, can acutely cause altered calcium cycling and cardiomyocyte relaxation through sodium pump inhibition (10). The following studies were performed to further examine how cardiac growth and function are chronically modified by the uremic milieu. Materials and Methods AnimalsMale Sprague-Dawley rats (200...

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“…Moreover, K ϩ adaptation seems to require an intact collecting duct, in particular a specific rise in Na ϩ , K ϩ -ATPase activity. 22 This is unrelated to aldosterone because the rise in Na ϩ , K ϩ -ATPase activity induced by K ϩ occurs in adrenalectomized animals. 23 Similarly, sheep on a high K ϩ intake achieve substantial increases in K ϩ excretion unrelated to either aldosterone or serum K ϩ .…”

Section: Discussionmentioning

confidence: 99%

Hyperkalemia, Renal Failure, and Converting-Enzyme Inhibition

García

Baigorria²,

Juncos³

2001

Hypertension

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Abstract-Hyperkalemia is widely viewed as a common complication of ACE inhibition in azotemic patients. These renal failure patients are the patients who benefit most from ACE inhibition. Because we could not confirm this notion after a retrospective evaluation of 236 azotemic patients, we studied 2 models of renal mass reduction. In the first, we did a 5/6 nephrectomy (Nx) on rats and studied them 2 weeks after surgery (before chronic renal changes had developed). A second group was studied 16 weeks after Nx, once chronic renal failure was established. Rats in both models were treated with quinapril in drinking water. After baseline evaluation, we challenged them either by a high-K ϩ diet or by blocking aldosterone receptors. We found that although quinapril blocked the K ϩ -induced increase in aldosterone, serum K ϩ levels and K ϩ balance were maintained before and during high K ϩ intake or during simultaneous spironolactone administration. We conclude that in hemodynamically stable rats with reduced renal mass and renal dysfunction, the administration of an ACE inhibitor does not cause severe hyperkalemia.

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Effect of chronic renal failure on Na,K-ATPase alpha 1 and alpha 2 mRNA transcription in rat skeletal muscle.

Cited by 29 publications

References 28 publications

Effects of recombinant human growth hormone on muscle protein turnover in malnourished hemodialysis patients.

Effects of recombinant human growth hormone on muscle protein turnover in malnourished hemodialysis patients.

Effect of Chronic Renal Failure on Cardiac Contractile Function, Calcium Cycling, and Gene Expression of Proteins Important for Calcium Homeostasis in the Rat

Hyperkalemia, Renal Failure, and Converting-Enzyme Inhibition

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