Abstract
Bladder hyperreflexia is a common non-motor feature of Parkinson’s disease. We now report on the contractility of the isolated primate detrusor strips devoid of nerve input and show that following MPTP, the amplitude and frequency of spontaneous contraction was increased. These responses were unaffected by dopamine D1 and D2 receptor agonists A77636 and ropinirole respectively. Contractions by exogenous carbachol, histamine or ATP were similar and no differences in the magnitude of noradrenaline-induced relaxation were seen in detrusor strip obtained from normal and MPTP-treated common marmosets (Callithrix jacchus). However, the neurogenic contractions following electrical field stimulation of the intrinsic nerves (EFS) were markedly greater in strips obtained from MPTP treated animals. EFS evoked non-cholinergic contractions following atropine were also greater but the contribution of the cholinergic innervation as a proportion of the overall contraction was smaller in the detrusor strips of MPTP treated animals, suggesting a preferential enhancement of the non-cholinergic transmission. Although dopaminergic mechanism has been proposed to underlie bladder hyperreflexia in MPTP-treated animals with intact bladder, the present data indicates that the increased neurogenically mediated contractions where no extrinsic innervation exists might be due to long-term adaptive changes locally as a result of the loss of the nigrostriatal output.
Highlights
Urinary dysfunction is common in Parkinson’s disease (PD) and takes the form of nocturia, frequency and urgency of micturition associated with detrusor hyperreflexia [1, 2]
Analysis of the tyrosine hydroxylase immunoreactivity in the substantia nigra showed a marked reduction in staining in all MPTP-treated animals (Fig 2)
Application of 1 mM adenosine triphosphate (ATP) led to a short-lasting contraction of the detrusor strips of the normal and MPTP-treated animals
Summary
Urinary dysfunction is common in Parkinson’s disease (PD) and takes the form of nocturia, frequency and urgency of micturition associated with detrusor hyperreflexia [1, 2]. Loss of dopaminergic nigro-striatal input is thought at least partially responsible for the hyperreflexia and imaging studies show changes in dopaminergic function in the striatum and in its output to the globus pallidus in individuals with PD and bladder dysfunction compared to those with PD and normal bladder function [3, 4]. Electrical stimulation of the substantia nigra and the direct injection of dopamine into the striatum can reverse these changes. In both man and in experimental models of PD, D1 dopamine agonists improve bladder hyperreflexia whereas D2 agonists either have no effect or make it worse.
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