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Beta-adrenergic responsiveness in hy...

MacDonnell, Scott M.

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Beta-adrenergic responsiveness in hypertension: Impact of exercise training.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Beta-adrenergic responsiveness in hypertension: Impact of exercise training./
作者:	MacDonnell, Scott M.
面頁冊數:	91 p.
附註:	Adviser: Joseph R. Libonati.
Contained By:	Dissertation Abstracts International67-09B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3233453
ISBN:	9780542870736

Beta-adrenergic responsiveness in hypertension: Impact of exercise training.
MacDonnell, Scott M.

Beta-adrenergic responsiveness in hypertension: Impact of exercise training. - 91 p.

Adviser: Joseph R. Libonati.

Thesis (Ph.D.)--Temple University, 2006.

Through the phosphorylation of key Ca2+ handling proteins, the beta-adrenergic receptor (beta-AR) cascade controls Ca2+ transients in the myocardium and thus the contractile state of the heart. Desensitization of this response in hypertension negatively impacts myocardial performance. We hypothesized that beta-AR responsiveness would be reduced in hypertension and augmented with moderate intensity aerobic exercise training. Our data showed that exercise training in hypertension reduced the beta-AR desensitizing kinase, GRK2, and improved peak left ventricular response to beta-AR stimulation, however failed to normalize beta-AR sensitivity. The protein phosphatase calcineurin is centrally involved in pressure overload myocardial hypertrophy and functionally has been shown to oppose beta-AR mediated phosphorylation of phospholamban. Therefore, we hypothesized that acute calcineurin inhibition with cyclosporine A (CsA) would normalize the reduced beta-AR sensitivity observed in the hypertensive myocardium, possibly by increasing phospholamban phosphorylation. CsA administration normalized the beta-AR desensitization observed in hypertension and negated differences in phospholamban phosphorylation found with beta-AR agonism alone (Ser16 and Thr17 ).

ISBN: 9780542870736Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Beta-adrenergic responsiveness in hypertension: Impact of exercise training.
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502 $a Thesis (Ph.D.)--Temple University, 2006.
520 $a Through the phosphorylation of key Ca2+ handling proteins, the beta-adrenergic receptor (beta-AR) cascade controls Ca2+ transients in the myocardium and thus the contractile state of the heart. Desensitization of this response in hypertension negatively impacts myocardial performance. We hypothesized that beta-AR responsiveness would be reduced in hypertension and augmented with moderate intensity aerobic exercise training. Our data showed that exercise training in hypertension reduced the beta-AR desensitizing kinase, GRK2, and improved peak left ventricular response to beta-AR stimulation, however failed to normalize beta-AR sensitivity. The protein phosphatase calcineurin is centrally involved in pressure overload myocardial hypertrophy and functionally has been shown to oppose beta-AR mediated phosphorylation of phospholamban. Therefore, we hypothesized that acute calcineurin inhibition with cyclosporine A (CsA) would normalize the reduced beta-AR sensitivity observed in the hypertensive myocardium, possibly by increasing phospholamban phosphorylation. CsA administration normalized the beta-AR desensitization observed in hypertension and negated differences in phospholamban phosphorylation found with beta-AR agonism alone (Ser16 and Thr17 ).
520 $a Chronic hypertension negatively impacts both myocardial structure and function by inducing concentric hypertrophy. We hypothesized that myocardial hypertrophy would be increased in hypertension and further augmented with exercise training. Utilizing both in vivo and in vitro measurement techniques, our data showed that cardiomyocyte cross sectional area, length, and width were increased in hypertension and greatest with exercise training superimposed on hypertension. Despite the increased myocardial hypertrophy observed with exercise training in hypertension, calcineurin abundance was reduced with training suggesting alternate pathways are involved in exercise mediated myocardial growth.
520 $a Collectively, exercise training enhanced peak beta-AR responsiveness and hypertrophy in the hypertensive myocardium. Exercise training reduced GRK2 abundance and increased the downstream phosphorylations of key Ca 2+ handling proteins. Additionally, acute calcineurin inhibition normalized left ventricular myocardial performance during stress in the hypertensive heart. The identification of calcineurin as a new molecular mechanism associated with the downregulation of the beta-AR cascade may contribute to the development of new therapeutic strategies in the treatment of hypertension.
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