Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys

Background Autonomic dysfunction is a well‐known dominant symptom in the advanced stages of Parkinson's disease. However, the role of cardiac sympathetic nerves still needs to be elucidated. Objectives To evaluate cardiac sympathetic response in Parkinsonian and dyskinetic monkeys. Methods Adult male monkeys were divided into 1 of the following 3 groups: controls, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine–treated monkeys, and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine+levodopa–treated animals. Noradrenaline, its metabolite normetanephrine, and phospho‐Heat shock proten 27 (p‐Hsp27) at serine 82 levels were analyzed in the left and right ventricles of the heart. Tyrosine hydroxylase immunohistochemistry was performed in the ventral mesencephalon. Results The results were the following: (1) 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine intoxication significantly increased normetanephrine levels and decreased noradrenaline turnover in the right ventricle without changes in the left ventricle; however, (2) levodopa treatment decreased noradrenaline levels and enhanced the normetanephrine/noradrenaline ratio in parallel with a very significant increase of Hsp27 activity in both ventricles. Conclusions Levodopa treatment could induce protective cardiac effects through the increased Hsp27 activity. © 2019 International Parkinson and Movement Disorder Society