Adrenergic ligands are endogenous proteins that modulate and evoke specific cardiovascular effects.
Adrenergic antagonists reverse the natural cardiovascular effect, based on the type of adrenoreceptor being blocked.
For example, if the natural activation of the α1-adrenergic receptor leads to vasoconstriction, an α1-adrenergic antagonist will result in vasodilation.
While the antagonists for alpha and beta receptors are usually different compounds, there has been recent drug development that effects both types of the adrenoreceptors.
Since this response, which is mostly seen as an increase in blood pressure, is produced by the release of the endogenous adrenergic ligands, administration of an adrenergic antagonist results a decrease in blood pressure, which is controlled by both heart rate and vasculature tone.
[14] Administration of an adrenergic antagonist that specifically targets the beta receptors, results in this decrease in blood pressure by slowing or reducing cardiac output.
Alpha-adrenergic antagonists are also used for treatment of ureteric stones, pain and panic disorders, withdrawal, and anesthesia.
[19] While these adrenergic antagonists are used for treating cardiovascular disease, mainly hypertension, they can evoke harmful cardiac events through prolongation of the QT interval.
Some adrenergic antagonists have a diminished ability to reduce stroke compared to placebo drugs.
When overused, adrenergic antagonists can result in bradycardia, hypotension, hyperglycemia and even hypodynamic shock.
If these adrenergic receptors are blocked too often, there will be an excess in calcium channel inhibition, which causes most of these problems.