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Cardiovascular effects of felypressin.
Rodrigo Cecanho1, Laurival Antonio De Luca, José Ranali
1Dentistry School São Leopoldo Mandic, Campinas, Brazil. rodrigocecanho@slmandic.com.br
Anesthesia Progress
|December 21, 2006
Summary
Felypressin (FEL) and vasopressin (AVP) cause cardiovascular effects via V1 receptors, with central V1 receptors and area postrema influencing pressor responses. FEL
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Neuroscience
Background:
- Felypressin (FEL) is a vasopressin analog with vasoconstrictive properties.
- Understanding the cardiovascular effects of FEL is crucial for its clinical application.
- The role of V1 receptors and central pathways in FEL's cardiovascular actions requires elucidation.
Purpose of the Study:
- To investigate the cardiovascular effects of felypressin (FEL) in Wistar rats.
- To determine the involvement of V1 receptors and the area postrema in FEL-induced cardiovascular responses.
- To compare the cardiovascular profile of FEL with vasopressin (AVP) and epinephrine (EPI).
Main Methods:
- Cardiovascular parameters (heart rate, mean arterial pressure) were measured in awake rats.
- Rats were treated with FEL, AVP, or EPI.
- Pharmacological interventions included intravenous (IV) and intracerebroventricular (ICV) V1 receptor antagonists, area postrema removal, and sham surgery.
- Statistical analysis employed Analysis of Variance (ANOVA) and Student-Newman-Keuls test.
Main Results:
- Both FEL and AVP induced pressor effects and bradycardia, which were inhibited by IV V1 antagonist.
- ICV V1 antagonist and area postrema removal potentiated the pressor effects of FEL and AVP.
- Epinephrine produced a greater pressor effect and similar bradycardia, unaffected by the tested interventions.
- A strong correlation between bradycardia and mean arterial pressure variation was observed for FEL, dependent on central V1 receptors and area postrema.
Conclusions:
- Felypressin mediates its pressor and bradycardic effects through V1 receptors.
- Central V1 receptors and the area postrema play a significant role in modulating FEL's cardiovascular actions.
- FEL's cardiovascular effects appear potentially less detrimental than those of epinephrine.
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