Left ventricular geometry and endogenous ouabain in a Flemish population

Kuznetsova, Tatiana; Manunta, Paolo; Casamassima, N.; Messaggio, Elisabetta; Jin, Yu; Thijs, Lutgarde; Richart, Tom; Fagard, Robert; Bianchi, Giuseppe; Staessen, Jan A.

doi:10.1097/hjh.0b013e32832e49a8

Cited by 14 publications

(18 citation statements)

References 37 publications

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“…Subsequently, several groups were successful in the isolation and purification of two distinct classes of endogenous CS, cardenolides and bufadienolides, from multiple mammalian tissues (2,14,19,28,29). Importantly, clinical studies have identified above normal circulating levels of ouabain/digitalis-like factor in diverse pathological conditions (2,3,12,15,27,35). Circulating CS levels are strongly correlated with the extent of left ventricular (LV) remodeling and impairment of LV function, implying a definitive pathophysiological role for this new class of steroid hormones.…”

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confidence: 99%

Mice expressing ouabain-sensitive α1-Na,K-ATPase have increased susceptibility to pressure overload-induced cardiac hypertrophy

Wansapura

Lasko

Lingrel

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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The Na,K-ATPase is a ubiquitous transmembrane pump and a specific receptor for cardiac glycosides such as ouabain and digoxin, which are used in the management of congestive heart failure (CHF). A potential role for these so-called endogenous cardiotonic steroids (CS) has been explored, and it has become apparent that such compounds are elevated and may play an important role in a variety of physiological and pathophysiological conditions such as hypertension and CHF. Recent evidence suggests that the Na,K-ATPase may act as a signal transducer upon CS binding and induce nonproliferative cardiac growth, implicating a role for endogenous CS in the development of cardiac hypertrophy and progressive failure of the heart. In the present study, we tested whether hypertrophic responses to pressure overload would be altered in mutant mice that specifically express ouabain-sensitive or ouabain-resistant α1- and α2-Na,K-ATPase subunits, as follows: α1-resistant, α2-resistant (α1(R/R)α2(R/R)); α1-sensitive, α2-resistant (α1(S/S)α2(R/R)); and α1-resistant, α2-sensitive (α1(R/R)α2(S/S), wild-type). In α1(S/S)α2(R/R) mice, pressure overload by transverse aortic coarctation induced severe left ventricular (LV) hypertrophy with extensive perivascular and replacement fibrosis at only 4 wk. Responses in α1(R/R)α2(S/S) and α1(R/R)α2(R/R) mice were comparatively mild. Mutant α1(S/S)α2(R/R) mice also had LV dilatation and depressed LV systolic contractile function by 4 wk of pressure overload. In separate experiments, chronic Digibind treatment prevented the rapid progression of cardiac hypertrophy and fibrosis in α1(S/S)α2(R/R) mice. These data demonstrate that mice with a ouabain-sensitive α1-Na,K-ATPase subunit have a dramatic susceptibility to the development of cardiac hypertrophy, and failure from LV pressure overload and provide evidence for the involvement of endogenous CS in this process.

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confidence: 99%

Mice expressing ouabain-sensitive α1-Na,K-ATPase have increased susceptibility to pressure overload-induced cardiac hypertrophy

Wansapura

Lasko

Lingrel

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…In smokers, median tobacco use was 12 cigarettes per day (interquartile range: 7-20). In regular drinkers, the median alcohol consumption was 11 g/day (interquartile range: [8][9][10][11][12][13][14][15][16][17][18][19][20].…”

Section: Results Study Populationmentioning

confidence: 99%

“…One experienced observer (T.K.) performed all echocardiograms 10 according to the recommendations of the American Society of Echocardiography, 11 using a Vivid 7 Pro (GE Vingmed, Horten, Norway) interfaced with a 2.5-3.5 MHz phased-array probe. The observer obtained M-mode echocardiograms of the LV from the parasternal long-axis view guided by two-dimensional image.…”

Section: Methodsmentioning

confidence: 99%

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Association of left ventricular mass with the AGTR1 A1166C polymorphism

Jin

Kuznetsova

Thijs

et al. 2012

American Journal of Hypertension

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“…Furthermore, EO modulates Na + /K + -ATPase in the vascular bed decreases vascular compliance by increasing smooth muscle tone [7,10] and this effect is ouabain specific [11]. In the heart, EO activated though Na + /K + -ATPase generated Src-kinase second messenger pathway promotes cardiomyocyte hypertrophy [12]. Observational data in naïve hypertensive patients revealed that elevated EO concentrations are associated with increased diastolic blood pressure and left ventricular hypertrophy [13].…”

Section: Introductionmentioning

confidence: 99%

Endogenous Ouabain Changes Rapidly During Cardiac Pulmonary by Pass

Bignami¹

2013

J Steroids Horm Sci

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Objective: Endogenous Ouabain (EO) is a cardiac glycoside secreted from the adrenal glands that plays a role sodium homeostasis with hemodynamic and renal effects. It is considered a stress hormone. The role of EO during critical illness is unknown.Aim: to study 1. the time course of EO during cardio pulmonary bypass (CPB) and 2. the ability of renal replacement therapy (RRT) to remove EO.Methods: in 11 patients undergoing mitral valve repair were performed an intraoperative time course with serial blood samples for EO, serum creatinine, NT-proBNP and cathecolamines. During surgery blood samples were repeated every 15 minutes. Then all these biomarkers were dosed at the end of surgery, 4 hours and 24 hours later. In the 15 patients undergoing EO time course during RRT, EO plasma levels were measured when AKI (Acute Kidney Injury) occurred (at R of RIFLE and 24 hours after this moment). Results:In patients undergoing mitral valve repair EO levels increased 15 minutes after the beginning of CPB reaching the peak 4 hours after surgery (from 198±10 to 350±130 pmol/L, p<0.0001). Circulating catecholamine (Norepneephrine ad Epinephrine) levels increased immediately after CBP. NT-proBNP increased only 4 hours after surgery, reaching high plasma levels when EO decreased. Plasma EO and creatinine levels resulted significantly directly related (r=0.45, p=0.01) after surgery. Continuous RRT did not modified circulating EO in AKI patients. Conclusion:EO may be considered a stress hormone that changes rapidly during acute volume expansion and blood pressure fall during CPB.Citation: Bignami E, Casamassima N, Frati E, Messaggio E, Corno L, et al. (2011) Endogenous Ouabain Changes Rapidly During Cardiac Pulmonary by Pass. J Steroids Hormon Sci S3:002.

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Left ventricular geometry and endogenous ouabain in a Flemish population

Cited by 14 publications

References 37 publications

Mice expressing ouabain-sensitive α1-Na,K-ATPase have increased susceptibility to pressure overload-induced cardiac hypertrophy

Mice expressing ouabain-sensitive α1-Na,K-ATPase have increased susceptibility to pressure overload-induced cardiac hypertrophy

Association of left ventricular mass with the AGTR1 A1166C polymorphism

Endogenous Ouabain Changes Rapidly During Cardiac Pulmonary by Pass

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