From the Guidelines
Adrenaline (epinephrine) primarily causes vasoconstriction by binding to alpha-1 adrenergic receptors on vascular smooth muscle, leading to immediate narrowing of blood vessels, especially in the skin, mucous membranes, and kidneys, as supported by the 2018 study on vasoactive agents in shock 1.
Mechanism of Action
Adrenaline's effects are rapid, helping redirect blood flow to vital organs during stress or "fight-or-flight" situations. However, adrenaline can also cause vasodilation in skeletal muscles and the liver through beta-2 receptor activation.
Comparison with Cortisol
Cortisol, a steroid hormone, has more complex effects on blood vessels that develop over hours rather than seconds. It enhances the sensitivity of blood vessels to other vasoconstrictors like adrenaline and angiotensin II, potentiating their effects.
Key Effects of Cortisol
Cortisol also reduces production of vasodilators like nitric oxide and prostacyclin, further promoting vasoconstriction. Additionally, cortisol increases blood pressure by increasing blood volume through sodium and water retention.
Clinical Implications
These complementary actions help maintain blood pressure during stress, with adrenaline providing immediate responses and cortisol sustaining these effects over longer periods, as noted in the 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care 1.
Other Vasoactive Agents
Other agents like norepinephrine, phenylephrine, dopamine, dobutamine, and milrinone also have vasoconstrictive or vasodilatory effects, but their mechanisms and uses differ, as discussed in the context of shock treatment 1.
Key Points
- Adrenaline causes immediate vasoconstriction through alpha-1 adrenergic receptors.
- Cortisol has sustained effects on blood vessels, enhancing vasoconstrictor sensitivity and reducing vasodilator production.
- Both hormones play critical roles in maintaining blood pressure during stress, with adrenaline providing rapid responses and cortisol sustaining effects over time.
From the FDA Drug Label
The mechanism of the antihypertensive effect of propranolol has not been established Among the factors that may be involved in contributing to the antihypertensive action include: (1) decreased cardiac output, (2) inhibition of renin release by the kidneys, and (3) diminution of tonic sympathetic nerve outflow from vasomotor centers in the brain Although total peripheral resistance may increase initially, it readjusts to or below the pretreatment level with chronic use of propranolol.
The effect of cortisol and adrenaline (epinephrine) on blood vessel vasoconstriction is not directly addressed in the provided drug label. However, it can be inferred that adrenaline (epinephrine), a beta-adrenergic receptor-stimulating agent, may cause vasodilation when it stimulates beta-adrenergic receptors. The drug label states that propranolol, a beta-adrenergic receptor-blocking agent, decreases the vasodilator responses to beta-adrenergic stimulation. However, the label does not provide information on how cortisol and adrenaline (epinephrine) affect blood vessel vasoconstriction. 2
From the Research
Cortisol and Adrenaline Effects on Blood Vessel Vasoconstriction
- Cortisol has been shown to increase blood pressure in humans through various mechanisms, including mineralocorticoid mimetic activity, alterations in peripheral and renovascular resistance, and vascular remodeling 3, 4, 5.
- The hypertensive effects of cortisol are accompanied by sodium retention and volume expansion, but co-administration of the type I (mineralocorticoid) receptor antagonist spironolactone does not prevent the onset of cortisol-induced hypertension 4.
- Cortisol-induced hypertension is not mediated by increased sympathetic tone, and preliminary evidence suggests that suppression of the nitric oxide system may play a role in cortisol-induced hypertension 4.
- Adrenaline (epinephrine) is not directly mentioned in the provided studies as a factor in blood vessel vasoconstriction in the context of cortisol effects.
- However, it is known that adrenaline can cause blood vessel vasoconstriction, but the provided studies do not discuss the interaction between cortisol and adrenaline in this context.
- The studies focus on the effects of cortisol on blood pressure and hypertension, and the mechanisms involved in cortisol-induced hypertension, including its effects on renal function, electrolyte metabolism, and atrial natriuretic peptide 6, 5, 7.
- Treatment options for hypertension in Cushing's syndrome, a condition characterized by elevated cortisol levels, include mineralocorticoid receptor antagonists, Ang II blockers, and ACE inhibitors, which may help reduce blood pressure in patients with CS 3, 5.