## 1 Introduction  
The association of vasoconstretricors with local anesthetics has the effect of counteracting the vasodilation caused by these drugs and increasing the permanence of the anesthetic solution in the area of the nerve to be blocked. However, they will be absorbed into the bloodstream and distributed to all tissues. The most used in clinical practice are sympathomimetic drugs such as epinephrine, noradrenaline, levonordephrine, and phenylephrine. Another group, less studied, is the synthetic derivative of vasopressin, felypressin [1, 2, 3].  
In dental practice, tricyclic antidepressants such as amitriptyline have been successfully used in the treatment of chronic orofacial pain, especially in cases of temporomandibular disorders [4, 5, 6, 7, 8]. On the other hand, vasoconstretricors associated with local anesthetics may have their systemic action potentiated by this pharmacological group, due to the increase in monoaminergic neurotransmission [9].  
Authors have reported a possible interaction, such as protriptyline with noradrenaline and epinephrine [10], imipramine with phenylephrine, noradrenaline, and epinephrine [11] and in dogs, desipramine with epinephrine, noradrenaline, and levonordephrine [12]. Recent literature reviews report the possible interaction, especially with epinephrine, [13, 14] warning and limiting the dose to 0.054 mg, due to its dose-dependent effects, in addition to the administration of the anesthetic solution being performed slowly, in small volumes [12].  
Epinephrine is certainly the one that promotes more tachycardia, while levonordefrin promotes more intense vasoconstriction, which could cause a great increase in blood pressure [15; 16]. Sympathomimetic drugs act on alpha and beta-adrenergic receptors, located in virtually all body tissues, with emphasis on alpha-1 receptors in blood vessels and beta-1 receptors in the heart. Their activation leads, respectively, to vasoconstriction and an increase in heart rate. These two effects are directly responsible for the elevation of blood pressure. On the other hand, beta-2 receptors are widely found in resistance vessels located in skeletal muscles and their activation causes them to dilate, diverting blood flow to important areas during the stress response.  
Phenylephrine is a selective alpha-1 agonist, causing vasoconstriction without, however, interfering with myocardial contractility. Something similar occurs with felypressin, a vasopressin V1A receptor agonist [3; 17; 18] which also does not bind to cardiac beta-1 receptors, not promoting tachycardia. This fact could imply a lower hypertensive action, giving these substances a prominent role when used in patients with different heart diseases.  
The present study was designed to simulate a situation closer to that experienced by dental professionals, to evaluate cardiovascular parameters after infiltration of different vasoconstretrics in an appropriate animal model. On the other hand, we also tried to simulate an accidental situation, where such vasoconstretric substances would be injected directly into the bloodstream. Therefore, the present study hypothesizes that the hypertensive action of vasoconstretrics associated with local anesthetics will not be potentiated by amitriptyline, demonstrating the safety of these substances.