Table 3.
Cardiovascular phenotype of mice carrying genetic modifications of different α1-adrenergic receptor subtypes.
| Receptor | Genetic modification | Phenotype | Ref. |
|---|---|---|---|
| α1b | Gene deletion | ↓ Resting blood pressure | 48 |
| ↓ Blood pressure response to phenylephrine | |||
| α1a | Overexpression/heart-specific promoter | ↑ Contractile response | 54 |
| ↑ Survival | |||
| ↑ ANF mRNA | |||
| No hypertrophy | |||
| ↑ Post-ischemic protection | |||
| α1b | Gene deletion | Normal resting blood pressure | 45 |
| ↓ Blood pressure response to phenylephrine | |||
| ↓ Vasoconstriction | |||
| α1b | Overexpression/heart-specific promoter | ↑ Phospholipase C activity | 55 |
| ↑ ANF mRNA | |||
| No hypertrophy | |||
| ↓ Contractile and heart rate response to β-AR | |||
| CAM α1b | Overexpression/heart-specific promoter | ↑ Phospholipase C activity | 50 |
| ↑ Hypertrophy | |||
| ↑ ANF mRNA | |||
| Normal blood pressure | |||
| CAM α1b | Overexpression/receptor promoter | ↓ Contractile response to β-AR | 52 |
| Autonomic failure | |||
| ↑ Hypertrophy | |||
| α1a α1b | Double gene deletion | In malesNormal resting blood pressure | 53 |
| ↓ Cardiac growth after birth | |||
| ↓ Heart rate, ↓ cardiac output | |||
| ↓ Basal ERK activity | |||
| ↑ Mortality to pressure overload | |||
| Contraction abnormalities | |||
| α1d | Gene deletion | ↓ Resting blood pressure | 49 |
| ↓ Blood pressure response to phenylephrine | |||
| ↓ Vasoconstriction | |||
| α1d α1b | Double gene deletion | ↓ Resting blood pressure | 57 |
| ↓↓ Blood pressure response to phenylephrine | |||
| ↓↓ Vasoconstriction |