Diabetic cardiomyopathy in rats: biochemical mechanisms of increased tolerance to calcium overload

Ziegelhöffer, A; Ravíngerová, T; Styk, J; Tribulová, N; Volkovová, Katarı́na; Seboková, J; Breier, Albert

doi:10.1016/0168-8227(96)01236-3

Cited by 26 publications

(17 citation statements)

References 15 publications

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“…Previously published studies documented that in acute STZ-induced diabetes lasting 7-10 days the reduction represented 10-22% in male rats (Davel et al 2000;Javorková et al 2009). Four-six weeks after the STZ treatment, body weight was significantly reduced by 34% (Michea et al 2001) and after 9 weeks the reduction yielded 30% (Ziegelhöffer et al 1996). Prolongation of STZ-induced diabetes to 16 weeks was followed by 56% decrease in body weight of males (Vrbjar et al 2004).…”

Section: Discussionmentioning

confidence: 90%

Influence of sub-chronic diabetes mellitus on functional properties of renal Na+,K+-ATPase in both genders of rats

Javorková¹,

Mezesova²,

Vlkovičová³

et al. 2010

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Abstract. For characterization of Na + ,K + -ATPase, a key enzyme involved in maintenance of intracellular sodium homeostasis, expression of α1 subunit and the ATP-and Na + -binding properties were investigated by Western blot analysis and by enzyme kinetics, respectively. Previous studies documented time-dependent alteration of properties of renal Na + ,K + -ATPase from its mobilization after 8 days to serious deteriorations after 16 weeks of diabetes in rats. Characterizing the critical period during development of the disease, when mobilization of Na + ,K + -ATPase observed in the acute phase turns to its damage, we examined the enzyme properties after 8 weeks lasting diabetes which was induced by a single intraperitoneal administration of streptozotocin in a dose of 65 mg·kg -1 . The unchanged expression of Na + ,K + -ATPase α1-subunit in both genders indicates that 8 weeks represent the time when the mobilization of enzyme synthesis observed previously in acute diabetes is lost. In this time the renal Na + ,K + -ATPase undergoes structural changes in the vicinity of Na + -binding site resulting in worsened affinity to sodium in both genders as indicated by 13% and 18% increase of K Na value in female and male rats, respectively. However, gender specific was the diabetes-induced decrease in affinity to ATP by 18% which occurred in female rats only.

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Section: Discussionmentioning

confidence: 90%

Influence of sub-chronic diabetes mellitus on functional properties of renal Na+,K+-ATPase in both genders of rats

Javorková¹,

Mezesova²,

Vlkovičová³

et al. 2010

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“…Accompanied by cardiac function loss, myocytes are in condition of calcium overload [8]. Several previous studies confirmed that the resting intracellular calcium ([Ca 2+ ]i) increased dramatically in both myocytes isolated from diabetic rats and myocytes incubated with high-glucose medium [9].…”

Section: Introductionmentioning

confidence: 96%

Protein kinase RNA-like endoplasmic reticulum kinase (PERK)/calcineurin signaling is a novel pathway regulating intracellular calcium accumulation which might be involved in ventricular arrhythmias in diabetic cardiomyopathy

Liu

Cai

Zhu

et al. 2014

Cellular Signalling

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“…The streptozotocin [STZ]-induced diabetes and NOdeficient hypertension are widely used experimental models for the investigation of heart failure [1][2][3][4]. Cardiac dysfunction in both models is consequence of different signal and metabolic derangement which continuously results in structural remodelling of cardiovascular system.…”

Section: Introductionmentioning

confidence: 99%

Ultrastructure and histochemistry of rat myocardial capillary endothelial cells in response to diabetes and hypertension

et al. 2005

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Insufficient growth and rarefaction of capillaries, followed by endothelial dysfunction may represent one of the most critical mechanisms involved in heart damage. In this study we examined histochemical and ultrastructural changes in myocardial capillary endothelium in two models of heart failure streptozotocin-induced diabetes mellitus (STZ) and NOdeficient hypertension in male Wistar rats. Diabetes was induced by a single i.v. dose of STZ (45 mg/kg) and chronic 9-week stage was analysed. To induce NO-deficient hypertension, animals were treated with inhibitor of NO synthase Lnitroarginine methylester (L-NAME) (40 mg/kg) for 4 weeks. Left ventricular tissue was processed for enzyme catalytic histochemistry of capillary alkaline phosphatase (AlPh), dipeptidyl peptidase IV (DPP IV), and endothelial NO synthase/NADPH-diaphorase (NOS) and for ultrastructural analysis. In diabetic and hypertensive rats, lower/absent AlPh and DPP IV activities were found in focal micro-areas. NOS activity was significantly reduced and persisted only locally. Quantitative evaluation demonstrated reduction of reaction product intensity of AlPh, DPP and NOS by 49.50%, 74.36%, 20.05% in diabetic and 62.93%, 82.71%, 37.65% in hypertensive rats. Subcellular alterations of endothelial cells were found in heart of both groups suggesting injury of capillary function as well as compensatory processes. Endothelial injury was more significant in diabetic animals, in contrast the adaptation was more evident in hypertensive ones. Concluding: both STZ-induced diabetes-and NO-deficient hypertension-related cardiomyopathy were accompanied by similar features of structural remodelling of cardiac capillary network manifested as angiogenesis and angiopathy. The latter was however, predominant and may accelerate disappearance of capillary endothelium contributing to myocardial dysfunction.

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Diabetic cardiomyopathy in rats: biochemical mechanisms of increased tolerance to calcium overload

Cited by 26 publications

References 15 publications

Influence of sub-chronic diabetes mellitus on functional properties of renal Na+,K+-ATPase in both genders of rats

Influence of sub-chronic diabetes mellitus on functional properties of renal Na+,K+-ATPase in both genders of rats

Protein kinase RNA-like endoplasmic reticulum kinase (PERK)/calcineurin signaling is a novel pathway regulating intracellular calcium accumulation which might be involved in ventricular arrhythmias in diabetic cardiomyopathy

Ultrastructure and histochemistry of rat myocardial capillary endothelial cells in response to diabetes and hypertension

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