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Felypressin, a synthetic analogue of vasopressin (AVP), has been widely used as a substitute for epinephrine (EPI) in anesthetic solutions to promote local vasoconstriction during medical and dental practices. Because it has no interaction with adrenergic receptors, it is suggested that felypressin has fewer side effects than EPI. Hence, Felypressin causes fewer cardiovascular and metabolic side effects, and it has a higher median lethal dose (LD50) than EPI. However, the mechanisms and the receptors used by felypressin to induce cardiovascular effects are unknown, and very few studies have been conducted on its possible systemic effects.
Cardiovascular effects of felypressin (FEL) were studied in Wistar rats. Heart rate and mean arterial pressure measurements were taken in awake rats treated with vasopressin (AVP), FEL, or epinephrine (EPI). Each group received either an intravenous (IV) or an intracerebroventricular V1 receptor antagonist, saline, area postrema removal, or sham surgery. Analysis of variance and Student-Newman-Keuls (P < .05) were applied. Felypressin and AVP induced a pressor effect, and bradycardia was inhibited by IV V1 antagonist. Intracerebroventricular V1 antagonist and area postrema removal enhanced their pressor effects. Epinephrine induced a higher pressor effect and a similar bradycardia that was not affected by the treatments. It was concluded that FEL depends on V1 receptors to induce pressor and bradycardic effects, and that it produces a high relationship between bradycardia and mean arterial pressure variation depending on area postrema and central V1 receptors. These effects are potentially less harmful to the cardiovascular system than the effects of EPI.
Cecanho, R., De Luca Jr, L. A., & Ranali, J. (2006). Cardiovascular effects of felypressin. Anesthesia progress, 53(4), 119-125.