Beta-adrenergic stimulation and myocardial function in the failing heart
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Beta-adrenergic stimulation and myocardial function in the failing heart. / El-Armouche, Ali; Eschenhagen, Thomas.
In: HEART FAIL REV, Vol. 14, No. 4, 01.12.2009, p. 225-41.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Beta-adrenergic stimulation and myocardial function in the failing heart
AU - El-Armouche, Ali
AU - Eschenhagen, Thomas
PY - 2009/12/1
Y1 - 2009/12/1
N2 - The sympathetic nervous system provides the most powerful stimulation of cardiac function, brought about via norepinephrine and epinephrine and their postsynaptic beta-adrenergic receptors. More than 30 years after the first use of practolol in patients with heart failure beta blockers are now the mainstay of the pharmacological treatment of chronic heart failure. Many aspects of their mechanism of action are well understood, but others remain unresolved. This review focuses on a number of questions that are key to further developments in the field. What accounts for and what is the role of beta-adrenergic desensitization, a hallmark of the failing heart? Is part of this adaptation predominantly beneficial and should therefore be reinforced, another part mainly maladaptive and therefore a target for antagonists? Which lessons can be drawn from studies in genetically engineered mice, which from (pharmaco) genetic studies? Finally, what are promising targets downstream of beta-adrenergic receptors that go beyond the current neurohumoral blockade?
AB - The sympathetic nervous system provides the most powerful stimulation of cardiac function, brought about via norepinephrine and epinephrine and their postsynaptic beta-adrenergic receptors. More than 30 years after the first use of practolol in patients with heart failure beta blockers are now the mainstay of the pharmacological treatment of chronic heart failure. Many aspects of their mechanism of action are well understood, but others remain unresolved. This review focuses on a number of questions that are key to further developments in the field. What accounts for and what is the role of beta-adrenergic desensitization, a hallmark of the failing heart? Is part of this adaptation predominantly beneficial and should therefore be reinforced, another part mainly maladaptive and therefore a target for antagonists? Which lessons can be drawn from studies in genetically engineered mice, which from (pharmaco) genetic studies? Finally, what are promising targets downstream of beta-adrenergic receptors that go beyond the current neurohumoral blockade?
KW - Animals
KW - Heart Failure
KW - Humans
KW - Mice
KW - Mice, Knockout
KW - Myocardial Contraction
KW - Pharmacogenetics
KW - Receptors, Adrenergic, beta
U2 - 10.1007/s10741-008-9132-8
DO - 10.1007/s10741-008-9132-8
M3 - SCORING: Journal article
C2 - 19110970
VL - 14
SP - 225
EP - 241
JO - HEART FAIL REV
JF - HEART FAIL REV
SN - 1382-4147
IS - 4
ER -