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Table 4.

The two biological determinants of cardiac remodelling

Phenotypic changesEffects of mechanicsEffects of other factors
Mitochondrial function Altered (ischemia) 
Ca L-type calcium channel density ⇑ (catecholamines) 
Ca-ATPase of sarcoplasmic reticulum ⇓ ⇑ (ischemia) 
Angiotensin II receptor density ⇑ ⇓ (plasma angiotensin II) 
β1-adrenergic receptor density ⇓ ⇓ ⇓ (plasma catecholamines) 
Cardiac catecholamine stores ⇑ ⇓ (ischemia) 
Gαi-2 ⇑ (catecholamines) 
Collagen concentration ⇑ (multifactorial) 
Apoptotic markers ⇑ ⇑ (multifactorial) 
Phenotypic changesEffects of mechanicsEffects of other factors
Mitochondrial function Altered (ischemia) 
Ca L-type calcium channel density ⇑ (catecholamines) 
Ca-ATPase of sarcoplasmic reticulum ⇓ ⇑ (ischemia) 
Angiotensin II receptor density ⇑ ⇓ (plasma angiotensin II) 
β1-adrenergic receptor density ⇓ ⇓ ⇓ (plasma catecholamines) 
Cardiac catecholamine stores ⇑ ⇓ (ischemia) 
Gαi-2 ⇑ (catecholamines) 
Collagen concentration ⇑ (multifactorial) 
Apoptotic markers ⇑ ⇑ (multifactorial) 

These are examples of phenotypic changes initially induced by mechanical stretch that can be further modified in a radical manner by interventions generated either by the specific cause of cardiac remodelling, such as ischemia, or by hormones or peptides, thus creating complex and sometimes paradoxical patterns.

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