dynorphins and Thromboembolism

Recently it has been suggested that endogenous k-opioid receptors may have a physiopathological role in ischemia induced neurodegeneration. The aim of this research is to show that in experimental thromboembolic (obtained mechanically using microspheres injected in the carotid) and atherosclerotic pathologies (obtained through a special diet) there is a common mechanism which involves mediation by dynorphine and the receptor compartment considered. The results, obtained using receptor binding techniques, showed a statistically significant increase in the number of k-opioid receptors (Bmax) without variations in the affinity (Kd) for the 3H dynorphine. We can therefore support the hypothesis that these changes in the modulation of the dynorphinergenic system may be part of a mechanism causing early cerebrovascular damage which results from embolic insults and is a consequence of such metabolic risk factors as are activated by atherogenesis.

Topics: Animals; Arteriosclerosis; Brain Ischemia; Cerebral Cortex; Diet, Atherogenic; Dynorphins; Electroencephalography; Kinetics; Lipids; Microspheres; Rabbits; Receptors, Opioid; Receptors, Opioid, kappa; Thromboembolism