How will a mouse's blood pressure change when adrenaline levels in its blood rise? - briefly
Elevated adrenaline in a mouse triggers swift vasoconstriction and heightened cardiac output, resulting in an acute increase in arterial blood pressure. The rise occurs within seconds and can elevate pressure several‑fold above baseline.
How will a mouse's blood pressure change when adrenaline levels in its blood rise? - in detail
When catecholamine concentrations rise in a mouse’s circulatory system, the sympathetic nervous system is activated, leading to rapid cardiovascular adjustments. Epinephrine binds to α‑ and β‑adrenergic receptors on vascular smooth muscle and cardiac tissue, producing several measurable effects:
- Vasoconstriction of peripheral arterioles mediated by α₁‑receptors increases systemic vascular resistance, a primary driver of elevated arterial pressure.
- Enhanced cardiac contractility and heart rate through β₁‑receptor stimulation raise stroke volume and cardiac output, further contributing to pressure elevation.
- Redistribution of blood flow away from non‑essential organs toward skeletal muscle and brain, reinforcing the pressor response.
The net result is a prompt rise in systolic and diastolic pressures, typically observed within seconds of adrenaline release. Experimental recordings in laboratory mice show systolic values increasing by 20–40 mm Hg and diastolic values by 10–25 mm Hg, depending on the dose and route of administration. The magnitude of the response correlates with plasma epinephrine concentration; higher levels produce proportionally larger pressure increments until receptor saturation limits further change.
During prolonged exposure, compensatory mechanisms such as baroreceptor-mediated vagal activation may attenuate the initial surge, leading to a partial return toward baseline values. Nevertheless, acute spikes remain the dominant feature of the hemodynamic profile when adrenaline levels ascend.