Phenotypic changes . | Effects of mechanics . | Effects 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 changes . | Effects of mechanics . | Effects 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.