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Prapawadee Pirompol, Vassana Teekabut, Wattana Weerachatyanukul, Tepmanas Bupha-Intr, and Jonggonnee Wattanapermpool

prescribed level of testosterone for ergogenic aid has raised many concerns about the possible adverse effects. One important concern of testosterone action in patients and consumers is cardiac hypertrophy induction. Despite the beneficial effect on muscle

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Melissa F Jackson, Dung Luong, Dor Dor Vang, Dilip K Garikipati, James B Stanton, O Lynne Nelson, and Buel D Rodgers

et al . 1999 , Shyu et al . 2006 , George et al . 2010 ). Conversely, we have recently reported that myostatin negatively regulates physiological cardiac hypertrophy ( Rodgers et al . 2009 , Valdivia 2009 ) as myostatin null ( Mstn −/− ) mice

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S Jeson Sangaralingham, M Yat Tse, and Stephen C Pang

Introduction Cardiac hypertrophy (CH) is an important predictor of cardiovascular morbidity and mortality, independent of other cardiovascular risk factors. The heart adapts in response to an array of mechanical, hemodynamic

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H Kobori, A Ichihara, Y Miyashita, M Hayashi, and T Saruta

We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin-angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague-Dawley rats was fixed by chronic angiotensin II infusion (40 ng/min, 28 days) via mini-osmotic pumps. Daily i.p. injection of thyroxine (0.1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri-iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0.12+/-0.03 and 0.15+/-0.03 microgram/h per liter, 126+/-5 and 130+/-5 ng/l respectively) (means+/-s.e.m.). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5.0+/-0.5 vs 3.5+/-0.1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74+/-2 vs 48+/-2%, 6.5+/-0.8 vs 3.8+/-0.4 ng/h per g, 231+/-30 vs 149+/-2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.

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Severe cardiac hypertrophy has been produced experimentally in rats by long-term, lowdose treatment with tri-iodothyroacetic acid. The dose used was insufficient to cause any apparent systemic or metabolic effect. It is suggested that similar iodinated substances in the blood in man, resulting from normal or abnormal thyroid hormone catabolism, may be causally related to some forms of cardiomyopathy.

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LG Fryer, MJ Holness, JB Decock, and MC Sugden

There is evidence for a role of protein kinase C (PKC) in the development of cardiac hypertrophy. We examined the expression of individual PKC isoforms in the adult rat heart in two distinct, well-characterised in vivo models of cardiac hypertrophy associated with an activated cardiac renin-angiotensin system, namely experimental hyperthyroidism and the TGR(mRen2)27 rat. The cardiac expression of a range of PKC isoforms (PKC-alpha, PKC-omega, PKC-epsilon, PKC-gamma, and PKC-tau) was examined by immuno-blotting. Our work demonstrates that the expression of total cardiac nPKC-omega and nPKC-epsilon relative to protein is selectively and differentially modified in these models. A consistent up-regulation of nPKC-omega in conjunction with overall down-regulation of nPKC-epsilon was observed in both models. The expression of other PKC isoforms was unaffected. The divergent responses of the expression of the two nPKC isoforms to an activated cardiac renin-angiotensin system in vivo in adulthood suggest that these individual nPKC isoforms subserve specific roles in the response.

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CJ Pemberton, TG Yandle, CJ Charles, MT Rademaker, GD Aitken, and EA Espiner

Whereas numerous studies have examined the cardiac tissue content and secretion of atrial natriuretic peptide (ANP), the response of brain natriuretic peptide (BNP) in states of experimental cardiac overload is less well documented. Our recent partial cloning of the ovine BNP gene has enabled us to study changes in cardiac tissue concentration, together with tissue and circulating molecular forms of ANP and BNP, in response to cardiac overload induced by rapid ventricular pacing (n = 7) and aortic coarctation (n = 6). In normal sheep, although highest levels of BNP were found in atrial tissue (15-fold those of the ventricle), the BNP/ANP concentration ratio in the ventricles was 10- to 20-fold higher than the ratio calculated for atrial tissue. Compared with normal sheep, significant depletion of both ANP and BNP concentrations within the left ventricle occurred after rapid ventricular pacing. Size exclusion and reverse phase HPLC analysis of atrial and ventricular tissue extracts from normal and overloaded sheep showed a single peak of high molecular weight BNP consistent with the proBNP hormone. In contrast, immunoreactive BNP extracted from plasma drawn from the coronary sinus was all low molecular weight material. Further analysis of plasma BNP using ion exchange HPLC disclosed at least 3 distinct immunoreactive peaks consistent with ovine BNP forms 26-29 amino acid residues in length. These findings show that BNP is stored as the prohormone in sheep cardiac tissues and that complete processing to mature forms occurs at the time of secretion. The capacity to process the prohormone at secretion is not impaired by chronic heart failure.

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Chun-Hsien Chu, Bor-Show Tzang, Li-Mien Chen, Chia-Hua Kuo, Yi-Chang Cheng, Ling-Yun Chen, Fuu-Jen Tsai, Chang-Hai Tsai, Wei-Wen Kuo, and Chih-Yang Huang

Introduction Cardiac hypertrophy can roughly be divided into two types: physiological and pathological ( Hunter & Chien 1999 ). In shorter stresses, physiological hypertrophy is an adaptive response to maintain heart function by increasing the size

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Chiung-Zuan Chiu, Bao-Wei Wang, and Kou-Gi Shyu

Introduction Cardiac hypertrophy and remodeling are considered to be compensatory processes in response to increased cardiac workload, caused by mechanical stress, hypertension, neurohumoral stimuli, myocardial injuries, or other environmental

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Bao-Wei Wang, Hang Chang, Peiliang Kuan, and Kou-Gi Shyu

Introduction Angiotensin II (AngII) plays a critical role in cardiac remodeling and promotes cardiac myocyte hypertrophy ( Schnee & Hsueh 2000 ). Excess of AngII can lead to cardiac dysfunction and failure. Myostatin is a transforming growth factor