Key result
Nitric oxide plays a major role in mediating the renal and peripheral vasodilatory responses induced by sustained exposure to platelet-activating factor in rats, but less so during transient exposure.
Why the study?
Does endogenous nitric oxide mediate the renal and systemic vasodilatory responses to platelet-activating factor in anesthetized rats?
Population
Anesthetized rats
Comparison
Platelet-activating factor administered via… vs Absence of NO synthase inhibition
Design
Preclinical
Authors
Loading...
Rat model implicates nitric oxide in sustained PAF vasodilation; leaves open translation to human vascular physiology.
Does endogenous nitric oxide mediate the renal and systemic vasodilatory responses to platelet-activating factor in anesthetized rats?
Nitric oxide plays a major role in mediating renal and peripheral vasodilatory responses during sustained, but not transient, exposure to platelet-activating factor in rats.
Handa et al. (2003) studied this question. Platelet-activating factor (PAF) with or without NO synthase inhibition vs. Control (absence of NO synthase inhibition or vasopressin-treated) was evaluated on Change in renal blood flow (RBF) and/or mean arterial blood pressure (MAP). Nitric oxide plays a major role in mediating the renal and peripheral vasodilatory responses induced by sustained exposure to platelet-activating factor in rats, but less so during transient exposure.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: