Atipamezole's low rate of side effects is due to its high specificity for ɑ₂-adrenergic receptors; it has very little affinity for ɑ₁-adrenergic receptors and no affinity for most serotonin, muscarinic, and dopamine receptors.
There is occasional vomiting, hypersalivation, and diarrhea.
It can potentially cause CNS excitement, which can lead to tremors, tachycardia (increased heart rate), and vasodilation.
The vasodilation leads to a transient decrease in blood pressure, which (in dogs) increases to normal within 10 minutes.
There have been reports of transient hypoxemia.
The chance of side effect can be minimized by administering atipamezole slowly.

There is a possibility of the sedation reversing abruptly, leading to nervous, aggressive, or delirious dogs.
Such cases are more associated with IV administration (which has a faster onset than IM administration).
The rapid administration of atipamezole leads to sudden displacement of dexmedetomidine from peripheral ɑ₂-adrenergic receptors; this can cause a sudden drop in blood pressure, which is followed by a reflex tachycardia and hypertension.

There have been some cases where IV administration of atipamezole lead to death via cardiovascular collapse.
This is thought to be combination of sudden hypotension added onto the low heart rate caused by sedatives.

There is some possibility of the animal relapsing into sedation after being given atipamezole, made more likely if the original sedative was given IV.

Rats and monkeys have experienced increased sexual activity after being given atipamezole.
Atipamezole's low rate of side effects is due to its high specificity for ɑ₂-adrenergic receptors; it has very little affinity for ɑ₁-adrenergic receptors and no affinity for most serotonin, muscarinic, and dopamine receptors. There is occasional vomiting, hypersalivation, and diarrhea. It can potentially cause CNS excitement, which can lead to tremors, tachycardia (increased heart rate), and vasodilation. The vasodilation leads to a transient decrease in blood pressure, which (in dogs) increases to normal within 10 minutes. There have been reports of transient hypoxemia. The chance of side effect can be minimized by administering atipamezole slowly.
There is a possibility of the sedation reversing abruptly, leading to nervous, aggressive, or delirious dogs. Such cases are more associated with IV administration (which has a faster onset than IM administration). The rapid administration of atipamezole leads to sudden displacement of dexmedetomidine from peripheral ɑ₂-adrenergic receptors; this can cause a sudden drop in blood pressure, which is followed by a reflex tachycardia and hypertension.
There have been some cases where IV administration of atipamezole lead to death via cardiovascular collapse. This is thought to be combination of sudden hypotension added onto the low heart rate caused by sedatives.
There is some possibility of the animal relapsing into sedation after being given atipamezole, made more likely if the original sedative was given IV.
Rats and monkeys have experienced increased sexual activity after being given atipamezole.
Atipamezole