Pressure overload

High pressure bellows Restriction ring Center-stem assembly Zero-setting screw High pressure overload seal Range-spring assembly Torque-tube assembly... 

Izumo, S., Nadal, G.B., Mahdavi, V. (1988). Protooncogene induction and reprogramming of cardiac gene expression produced by pressure overload. Proc. Natl. Acad. Sci. USA 85, 339-343. 

Pressure overload (e.g., systemic or pulmonary hypertension, aortic or pulmonic valve stenosis)... 

Causes of systolic dysfunction (decreased contractility) are reduction in muscle mass (e.g., myocardial infarction [MI]), dilated cardiomyopathies, and ventricular hypertrophy. Ventricular hypertrophy can be caused by pressure overload (e.g., systemic or pulmonary hypertension, aortic or pulmonic valve stenosis) or volume overload (e.g., valvular regurgitation, shunts, high-output states). 

In addition to its pump function, the heart is also a secretory organ. Cardiac cells produce two small peptides, the natriuretic factors, which oppose the vasoconstrictive actions of noradrenaline (norepinephrine) from the sympathetic nervous system and of the peptide angiotensin II. By causing vasodilation and natriuresis (increased excretion of sodium in the urine), atrial natriuretic peptide (ANP) secreted from the atria and B-type natriuretic peptide (BNP) secreted by both atria and probably more significantly, from the ventricles, reduce blood pressure. The stimulus to secretion of natriuretic peptides is wall stretch of the chambers of the heart, indicating volume and pressure overload of the vascular system. A third member of the natriuretic peptide family, CNP, is secreted by endothelial cells. 

Kwiatkowska-Patzer B, Domanska-Janik K (1991) Increased 19 kDa protein phosphorylation and protein kinase C activity in pressure-overload cariac hypertrophy. Basic Res Cardiol 86 402-409... 

A. Hara, K. Yuhki, T. Fujino, T. Yamada, K. Takayama, S. Kuriyama, O. Takahata, H. Karibe, Y. Okada, C.-Y. Xiao, H. Ma, S. Narumiya, F. Ushikubi, Augmented cardiac hypertrophy in response to pressure overload in mice lacking the prostaglandin I2 receptor. Circulation 112 (2005) 84. 

Duda, M., O Shea, K., Tintinu, A., Xu, W., Khairallah, R., Barrows, B., Chess, D., Azimzadeh, A., and Harris, W. (2009). Fish oil, but not flaxseed oil, decreases inflammation and prevents pressure overload-induced cardiac dysfunction. Cardiovasc. Res. 81,319-327. 

Ding, B., Price, R. L., Borg, T. K, Weinberg, E. O., Halloran, P. F., and Lorell, B. H. (1999). Pressure overload induces severe hypertrophy in mice treated with cyclosporine, an inhibitor of calcineurin. Circ. Res. 84, 729-734. 

Meguro, T., Hong, C., Asai, K., Takagi, G., McKinsey, T. A. et al. (1999). Cyclosporine attenuates pressure-overload hypertrophy in mice while enhancing susceptibility to decompensation and heart failure. Circ. Res. 84, 735-740. 

Akhtar SA, Luttrell RM, Rockman HA, Iaccarino G, Lefkowitz RJ, Joch WJ. 1998. Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy. Science 280 574-577. 

Holmer SR, Bruckschlegl G, Schunkert H, Rataj DB, Krower EP, Riegger GA. 1996. Functional activity and expression of the myocardial post-receptor adenylyl cyclase system in pressure-overload hypertrophy in rat. Cardiovasc Res 31 719-728. 

Longabaugh JP, Vatner DE, Vatner SF, Homey CJ. 1988. Decreased stimulatory guanosine triphosphate binding protein in dogs with pressure-overload left ventricular failure. J Clin Invest 81 420—424. 

Volume and Pressure Overload Hypertrophy-Induced Changes... 

Akers, W.S., Cross, A., Speth, R., Dwoskin, L.P., and Cassis, L.A. 2000. Renin-angiotensin system and sympathetic nervous system in cardiac pressure-overload hypertrophy. Am. J. Physiol. Heart Circ. Physiol. 279 H2797-H2806. 

Galinier, M., Senard, J.M., Valet, P., Arias, A., Daviaud, D., Clock, Y., Bounhoure, J.P., and Montastruc, J.L. 1994. Cardiac p-adrenoceptors and adenylyl cyclase activity in human left ventricular hypertrophy due to pressure overload. Fundam. Clin. Pharmacol. 8 90-99. 

Hamawaki, M., Coffman, T.M., Lashus, A., Koide, M., Zile, M.R., Oliverio, M.I., DeFreyte, G., Cooper, G. 4th, and Carabello, B.A. 1998. Pressure-overload hypertrophy is unabated in mice devoid of ATja receptors. Am. J. Physiol. 274 H868-H873. 

In vitro studies have demonstrated that the exposure of cardiac myocytes to either ET-1 or All promoted hypertrophy, the reexpression of cardiac fetal genes, and the downregulation of SERCA2 mRNA (Shubeita et al. 1990 Sadoshima and Izumo 1993 Calderone et al. 2000 Strait et al. 2001). In the pressure-overloaded heart, myocardial ET-1 expression was increased and the pharmacological antagonism of... 

Calcineurin expression, activation, and function in cardiac pressure-overload hypertrophy. Circulation 101 2431-2437. 

Mohabir, R., Young, S.D., and Strosberg, A.M. 1994. Role of angiotensin in pressure overload-induced hypertrophy in rats effects of angiotensin-converting enzyme inhibitors, an ATI receptor antagonist, and surgical reversal. J. Cardiovasc. Pharmacol. 23 291-299. 

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