Sex differences in the alterations of Na+,K+-ATPase following ischaemia-reperfusion injury in the rat kidney (original) (raw)
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Cellular and molecular biology (Noisy-le-Grand, France), 2014
Acute renal failure (ARF) induced by Ischemia-Reperfusion (I-R) is associated with a significant impairment of tubular sodium reabsorption. Na⁺,K⁺-ATPase has a crucial role in tubular sodium reabsorption and maintenance of water and ion homeostasis. In this study, we examined whether renal I-R affects Na⁺,K⁺-ATPase activity in a renal auto graft model (Large White Pig) with controlateral nephrectomy. Kidney samples were obtained from medulla (n = 4) and cortex (n = 3) after one hour of warm ischemia in autotransplanted models. These experimental groups were compared with a controlateral nephrectomy group (Control). Na⁺,K⁺-ATPase activity in purified membrane fractions was measured as ouabain-sensitive K⁺ -stimulated paranitrophenyl phosphatase (pNPPase) activity. The Na⁺,K⁺-ATPase activities of control, ischemia and ischemia -reperfusion were significantly higher in the medulla than in the cortex, irrespective of the experimental group (P<0.05). In cortices, Na⁺,K⁺-ATPase activit...
Acute diabetes mellitus and its influence on renal Na,K-ATPase in both genders
General Physiology and Biophysics, 2009
Due to the importance of renal Na,K-ATPase in maintaining the sodium homeostasis in the organism, its activity and abundance is intensively studied in condition of diabetes mellitus. The main subject of this study was the investigation of properties of renal Na,K-ATPase and abundance of its α1 subunit in view of possible gender-dependent differences in male and female diabetic rats. Diabetes was induced by a single intraperitoneal dose of streptozotocin in a dose of 65 mg·kg -1 . The acute diabetes lasting 8 days induced a significant increase in Na,K-ATPase activity accompanied by significant gender specific increase in K m value indicating a worsened affinity of ATP-binding site in female rats. In addition, our present experiments, revealed a significantly higher abundance of renal Na,K-ATPase α1 subunit in diabetic rats of both genders amounting 94% increase in males and 107% in females. But, not all of the newly synthesized enzyme molecules are fully active, as the increase in the number of active molecules is smaller (representing 23% in males and 20% in females) as indicated by lower increase in V max values.
Postischemic injury, delayed function and Na+/K+-ATPase distribution in the transplanted kidney
Kidney International, 1995
We evaluated the postischemic renal injury in 22 patients undergoing renal transplantation. Renal tissue obtained 45 to 60 minutes after reperfusion of the allograft was stained with specific antibodies against the delta subunit of Na+/K(+)-ATPase, fodrin and ankyrin. The distribution of each cytoskeletal protein was analyzed by laser confocal microscopy. Subsequent allograft function was assessed on two occasions, 1 to 3 and 36 hours post-reperfusion, respectively. Recipients were divided into two groups: those who achieved a normal GFR on post-transplant day 3 (group 1, N = 12) and those with persistent hypofiltration (group 2, N = 10). Patients of both groups exhibited impaired sodium reabsorption and isosthenuria one to three hours postoperatively, but these abnormalities persisted on day 3 only in group 2 subjects with persistent hypofiltration. Abnormalities of Na+/K(+)-ATPase, ankyrin and fodrin were confined to proximal tubule cells and were marked only in the subjects of group 2. They consisted of redistribution of each cytoskeletal protein from the basolateral membrane to the cytoplasm. We conclude that postischemic injury to a renal allograft results in a loss of polarity of proximal tubule cells. We propose that ensuing impairment of proximal sodium reabsorption could activate tubuloglomerular feedback, thereby contributing to the protracted hypofiltration that characterizes this form of postischemic, acute renal failure.
Renal Redox Balance and Na+, K+-ATPase Regulation: Role in Physiology and Pathophysiology
Oxidative Stress - Molecular Mechanisms and Biological Effects, 2012
This chapter begins with a brief introduction to the basic principles of renal function, Na + ,K +-ATPase structure and mechanisms of regulation, followed by a short review on renal reactive oxygen species production and anti-oxidant defence. An exploration of the new findings and ideas on the dynamic interplay between renal redox balance, the molecular effects at the cellular level and Na + ,K +-ATPase function is approached more deeply in the following section. Finally, experimental animal models supporting that loss of redox balance and altered Na + ,K +-ATPase function contribute to the development of renal associated pathologies is addressed. The chapter ends with a broad overview, given in the conclusion section. 2. The kidney function and Na + , K +-ATPase In an adult organism the kidney plays an important role in the regulation of blood pressure, nutrient and electrolyte reabsorption and drug and metabolite excretion. This is achieved due www.intechopen.com Oxidative Stress-Molecular Mechanisms and Biological Effects 158 to the presence of specialized proteins that are distributed into specific domains of the apical or basolateral membrane of the distinct nephron segments (Abdolzade-Bavil et al., 2004). Na + ,K +-ATPase is the major transporter of sodium ions in renal basolateral epithelia throughout the nephron and one of the most important renal transporters (Jaitovich & Bertorello, 2010). Na + ,K +-ATPase is an oligomeric transmembrane protein composed of two main subunits, and (Figure 1). The-subunit is the catalytic domain of Na + ,K +-ATPase and contains the binding site for sodium ions, potassium ions, ATP, steroid hormones and phosphorylation sites for protein kinase A and protein kinase C (
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2002
The effects of ischaemic injury and reperfusion on renal function, cortical ATP content, alkaline phosphatase activity and (Na +K )-ATPase activity and abundance in cortical homogenates and isolated basolateral and apical membranes were examined. Rats were submitted to 5 or 40 min of right renal artery occlusion and 60 min of reperfusion. Renal function of the ischaemic^reperfused kidney was studied by conventional clearance techniques. Our results show that 1 h of reperfusion after a short period of renal ischaemia (5 min) allows the complete restoration of the biochemical features of cortical cells and functional properties of the injured kidney. A longer period of ischaemia, such as 40 min, followed by 1 h of reperfusion showed functional and biochemical alterations. ATP recovered from 26% after 40 min of ischaemia to 50% of control values after 1 h reperfusion. However, renal function was strongly impaired. Brush border integrity was compromised, as suggested by AP excretion and actin appearance in urine. Although total cortical (Na +K )-ATPase activity was not different from controls, its distribution in isolated apical and basolateral membranes was abnormal. Remarkably, we detected an increase in K-subunit protein abundance that may suggest that (Na +K )-ATPase synthesis is promoted by ischaemia^reperfusion. This increase may play an important role in the pathophysiology of ischaemic acute renal failure. ß 0925-4439 / 02 / $^see front matter ß 2002 Elsevier Science B.V. All rights reserved. PII: S 0 9 2 5 -4 4 3 9 ( 0 1 ) 0 0 0 8 7 -4 * Corresponding