Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats

Stefanon, Ivanita; Cade, Jamil; Fernandes, Aurélia Araújo; Ribeiro, Rogério Faustino; Targueta, Gabriel Pelegrineti; Mill, José Geraldo; Vassallo, Dalton Valentim

doi:10.1590/s0100-879x2009005000015

Cited by 16 publications

(11 citation statements)

References 32 publications

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“…The enzymatic material that was used to determine whether lead exposure is capable of affecting Na + , K + -ATPase activity was extracted as described by Stefanon et al (2009) [22]. Ventricular tissue was homogenised in a solution containing Tris-HCl (20 mM) and EDTA (1 mM) at a pH of 7.5.…”

Section: Methodsmentioning

confidence: 99%

Chronic Lead Exposure Increases Blood Pressure and Myocardial Contractility in Rats

et al. 2014

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We investigated the cardiovascular effects of lead exposure, emphasising its direct action on myocardial contractility. Male Wistar rats were sorted randomly into two groups: control (Ct) and treatment with 100 ppm of lead (Pb) in the drinking water. Blood pressure (BP) was measured weekly. At the end of the treatment period, the animals were anaesthetised and haemodynamic parameters and contractility of the left ventricular papillary muscles were recorded. Blood and tissue samples were properly stored for further biochemical investigations. Statistical analyses were considered to be significant at p<0.05. The lead concentrations in the blood reached approximately 13 µg/dL, while the bone was the site of the highest deposition of this metal. BP in the Pb-treated group was higher from the first week of lead exposure and remained at the same level over the next four weeks. Haemodynamic evaluations revealed increases in systolic (Ct: 96±3.79 vs. Pb: 116±1.37 mmHg) and diastolic blood pressure (Ct: 60±2.93 vs. Pb: 70±3.38 mmHg), left ventricular systolic pressure (Ct: 104±5.85 vs. Pb: 120±2.51 mmHg) and heart rate (Ct: 307±10 vs. Pb: 348±16 bpm). Lead treatment did not alter the force and time derivatives of the force of left ventricular papillary muscles that were contracting isometrically. However, our results are suggestive of changes in the kinetics of calcium (Ca++) in cardiomyocytes increased transarcolemmal Ca++ influx, low Ca++ uptake by the sarcoplasmic reticulum and high extrusion by the sarcolemma. Altogether, these results show that despite the increased Ca++ influx that was induced by lead exposure, the myocytes had regulatory mechanisms that prevented increases in force, as evidenced in vivo by the increased systolic ventricular pressure.

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Section: Methodsmentioning

confidence: 99%

Chronic Lead Exposure Increases Blood Pressure and Myocardial Contractility in Rats

et al. 2014

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“…Inappropriate regulation of NKA activity leads to excessive loss of K + and gain of Na + by the cell. The NKA hypoactivity may modify the Na + , K + and Ca 2+ transport across the sarcolemma resulting in ventricular dysfunction [65]. In 2004, Dostanic et al have demonstrated that the a1 isoform of NKA regulates cardiac contractility, and that both the a1 and a2 isoforms are functionally and physically coupled with the Na/Ca exchanger in heart [66].…”

Section: Pathophysiological Relevance Of Nkamentioning

confidence: 99%

Na+, K+-ATPase: Ubiquitous Multifunctional Transmembrane Protein and its Relevance to Various Pathophysiological Conditions

Suhail

2010

J Clin Med Res

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The Na+, K+-ATPase (NKA) is an ubiquitous enzyme consisting of α, β and γ subunits, and is responsible for the creation and maintenance of the Na+ and K+ gradients across the cell membrane by transporting 3 Na+ out and 2 K+ into the cell. Sodium pump regulation is tissue as well as isoform specific. Intracellular messengers differentially regulate the activity of the individual NKA isozymes. Regulation of specific NKA isozymes gives cells the ability to precisely coordinate NKA activity to their physiological requirements. It is the only known receptor for the cardiac glycosides used to treat congestive heart failure and cardiac arrhythmias. Endogenous ligands structurally similar to cardiac glycosides may act as natural regulators of the sodium pump in heart and other tissues. Identification of naturally occurring regulators of NKA could initiate the discovery of new hormone-like control systems involved in the etiology of selected disease processes, hence the importance of understanding the relation of the sodium pump and its ligands to disease. Diabetes has a marked effect on the metabolism of a variety of tissues and because the NKA is critical for the membrane potential and many transports, a change in its activity in diabetes would have profound consequence in these tissues. NKA is also involved in hypertension, salt balance, cardiovascular and renal disorders, sperm capacitation, cell volume regulation, apoptosis, rheumatoid arthritis, sepsis, neurological disorders, lung edema clearance and preeclampsia. NKA activity and expression in the collecting duct of kidney are modulated physiologically by hormones like aldosterone, vasopressin, and insulin. NKA enzyme activity and subunit levels are reduced in carcinoma, NKA-β levels were highly reduced in an invasive form of human renal clear cell carcinoma, androgen-dependent prostate cancer, in early stages of urothelial cancer, as well as in poorly differentiated, highly motile carcinoma cell lines obtained from various tissues suggesting a functional link between reduced NKA-β expression and cancer progression. It could be a target for the development of anticancer drugs as it serves as a signal transducer, it is a player in cell adhesion and its aberrant expression and activity are implicated in the development and progression of different cancers.KeywordsNa+, K+-ATPase (NKA); Cardiotonic steroids (CTS); Diabetes; Hypertension; Cardiovascular and renal disorders; Signal transducer; Anticancer drugs

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“…To determine whether lead acetate (8 µM) can affect Na + ,K + -ATPase activity, enzymatic material was extracted as described by Stefanon et al 22. Ventricular tissue (n = 6 per group) was homogenized in a solution containing 20 mM Tris-HCl and 1 mM EDTA, pH 7.5.…”

Section: Methodsmentioning

confidence: 99%

Acute exposure to lead increases myocardial contractility independent of hypertension development

Fioresi

et al. 2013

Braz J Med Biol Res

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We studied the effects of the acute administration of small doses of lead over time on hemodynamic parameters in anesthetized rats to determine if myocardial contractility changes are dependent or not on the development of hypertension. Male Wistar rats received 320 µg/kg lead acetate iv once, and their hemodynamic parameters were measured for 2 h. Cardiac contractility was evaluated in vitro using left ventricular papillary muscles as were Na+,K+-ATPase and myosin Ca2+-ATPase activities. Lead increased left- (control: 112 ± 3.7 vs lead: 129 ± 3.2 mmHg) and right-ventricular systolic pressures (control: 28 ± 1.2 vs lead: 34 ± 1.2 mmHg) significantly without modifying heart rate. Papillary muscles were exposed to 8 µM lead acetate and evaluated 60 min later. Isometric contractions increased (control: 0.546 ± 0.07 vs lead: 0.608 ± 0.06 g/mg) and time to peak tension decreased (control: 268 ± 13 vs lead: 227 ± 5.58 ms), but relaxation time was unchanged. Post-pause potentiation was similar between groups (n = 6 per group), suggesting no change in sarcoplasmic reticulum activity, evaluated indirectly by this protocol. After 1-h exposure to lead acetate, the papillary muscles became hyperactive in response to a β-adrenergic agonist (10 µM isoproterenol). In addition, post-rest contractions decreased, suggesting a reduction in sarcolemmal calcium influx. The heart samples treated with 8 µM lead acetate presented increased Na+,K+-ATPase (approximately 140%, P < 0.05 for control vs lead) and myosin ATPase (approximately 30%, P < 0.05 for control vs lead) activity. Our results indicated that acute exposure to low lead concentrations produces direct positive inotropic and lusitropic effects on myocardial contractility and increases the right and left ventricular systolic pressure, thus potentially contributing to the early development of hypertension.

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Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats

Cited by 16 publications

References 32 publications

Chronic Lead Exposure Increases Blood Pressure and Myocardial Contractility in Rats

Chronic Lead Exposure Increases Blood Pressure and Myocardial Contractility in Rats

Na+, K+-ATPase: Ubiquitous Multifunctional Transmembrane Protein and its Relevance to Various Pathophysiological Conditions

Acute exposure to lead increases myocardial contractility independent of hypertension development

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