Related Experiment Videos
Platelet-activating factor antagonists increase vascular reactivity in perfused rat lungs
J Haynes1, S W Chang, K G Morris
1Cardiovascular Pulmonary Research Laboratory, University of Colorado Health Sciences Center, Denver 80262.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|November 1, 1988
Summary
Endogenous platelet-activating factor (PAF) helps control pulmonary circulation tone. Blocking PAF receptors increased baseline pressure and potentiated vasoconstriction, indicating PAF
Area of Science:
- Pulmonary circulation physiology
- Vascular pharmacology
- Platelet-activating factor (PAF) signaling
Background:
- Platelet-activating factor (PAF) exhibits vasodilatory properties at low doses in the pulmonary circulation.
- The role of endogenous PAF in regulating pulmonary vascular tone remains incompletely understood.
Purpose of the Study:
- To investigate the role of endogenous PAF in the control of pulmonary circulation tone.
- To determine if PAF receptor antagonists affect baseline pulmonary perfusion pressure and responses to vasoconstrictors.
Main Methods:
- Utilized isolated perfused rat lungs and in vivo animal models.
- Employed PAF receptor antagonists (SRI 63-441 and L659,989) to block PAF signaling.
- Assessed effects on baseline perfusion pressure, angiotensin II (ANG II)-induced vasoconstriction, and hypoxic pulmonary vasoconstriction (HPV).
Main Results:
- PAF receptor antagonists significantly increased baseline pulmonary perfusion pressure and potentiated ANG II and HPV.
- These potentiations were independent of circulating blood elements.
- Vasodilation in response to PAF was impaired by receptor blockade; combined cyclooxygenase inhibition and PAF blockade had additive effects on ANG II vasoconstriction but not HPV.
Conclusions:
- Endogenous PAF plays a significant vasodilatory role in maintaining normal tone in the pulmonary circulation.
- PAF signaling contributes to the regulation of pulmonary vascular responses to ANG II and hypoxia.