## 4 Discussion
Our findingscoincide with [PERSON] et al., who observed negligible effects on the cardiovascular system at doses that, based on body weight, would correspond to amounts used clinically [27]. Felypressin has very similar results to those shown by epinephrine in both groups of animals (Figure 1B), which places it as an important alternative non-adrenergic vasoconstration. According to the literature, felypressin should not increase heart rate, as it does not act on adrenergic receptors. Felypressin acts on a class of receptors called V1a. Under physiological conditions, the activation of this vascular receptor promotes vasoconstriction, which with our results it was possible to confirm [3; 28]. It is evident the great hypertensive effect of phenylephrine compared to the other vasoconstrators epinephrine and felypressin, after infiltration of equivalent doses (Figure 1A). Phenylephrine, being a specific alpha-1 receptor agonist, does not affect vascular beta-2 receptors as epinephrine does; this last agonist action on beta-2 adrenergic leads to great vasodilation in vessels located in skeletal muscles, which would somehow compensate for the agonist action on vascular alpha-1 and cardiac beta-1 receptors [29]. For this reason, the results of our study showed a great effect of this vasoconstrtictor, with a significant increase in blood pressure, especially with the higher doses used in this study. With the lowest dose of 2 tubes, there is no significant difference between the vasoconstrtictors, with a significant difference from the dose of 8 tubes between phenylephrine and epinephrine (* \(p<0.05\)), and only at the high dose of 32 tubes is there a significant difference among the three vasoconstrtictors in the control group. In the present study, the animals were treated with amitriptyline, a drug known to inhibit the membrane transport protein responsible for the reuptake of catecholamines (dopamine, noradrenaline and epinephrine). Phenylephrine differs chemically from noradrenaline in that it does not have a hydroxyl group at position 4 of the benzene ring, which causes this substance to have little affinity for the transporter protein responsible for the reuptake of catecholamines. As in our study, there was no stimulation of sympathetic nerves in the area, there was no release of the neurotransmitter, and phenylephrine does not seem to have an affinity for the transporter protein, it would be expected that its vasoconstrtictor action would not be potentiated by treatment with amitriptyline, as shown by our results. In the amitriptyline group (Figure 1B), the same effect of phenylephrine can be observed. The significance (* \(p<0.05\)) is only obtained from the dose of 8 tubes between the infiltration of phenylephrine and the other vasoconstrtictors, and between felypressin and epinephrine, there is no significant difference. Tricyclic drugs are known to be norepinephrine and serotonin reuptake inhibitors; as the infiltrated epinephrine is also recaptured by the same transporters, which are inhibited by the action of amitriptyline, this substance could remain longer bound to adrenergic receptors, causing a greater increase in blood pressure. When the three vasoconstrtictors were administered intravenous (Figure 2), the great increase in blood pressure promoted by all is evident, but especially by phenylephrine, even in small doses, highlighting the danger of accidental injection of this vasoconstritor into a patient's bloodstream. Corroborating our results with [PERSON] et al. [11]. Intravenous or subcutaneous injection of this vasoconstrtictor causes an increase in systolic and diastolic pressure, both in men and in other species. In our results, after intravenous injection of epinephrine (Figure 2A), treatment with amitriptyline did not influence blood pressure responses when we compared dose-response curves for the two groups of animals.