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Patients with Parkinson's disease (PD) exhibit both motor and non-motor symptoms. Among the non-motor symptoms, cardiovascular autonomic dysfunction is frequently observed. Here, we evaluated baroreflex function, vascular reactivity and neuroanatomical changes in brainstem regions involved in the neural control of circulation in the 6-hydroxydopamine (6-OHDA) model of PD. Male Wistar rats received a bilateral injection of 6-OHDA or vehicle into the striatum. After 61days, baroreflex function and vascular reactivity were assessed. The 6-OHDA and vehicle groups showed similar increases in mean arterial pressure (MAP) in response to phenylephrine (PE). However, the bradycardia observed in the vehicle group was blunted in the 6-OHDA-treated rats. Injection of sodium nitroprusside (SNP) decreased hypotension, tachycardia and vascular relaxation in 6-OHDA-treated rats. Bilateral intrastriatal 6-OHDA led to massive degeneration of tyrosine hydroxylase (TH)-immunoreactive neurons in the substantia nigra and to reductions in the numbers of A1/C1 and A5 catecholaminergic neurons while sparing A2 neurons within the nucleus of the solitary tract (NTS). 6-OHDA-treated rats also showed decreases in Phox2b-expressing neurons in the NTS and in choline acetyltransferase (ChAT) immunoreactivity in the nucleus ambiguus. Altogether, our data suggest that this model of PD includes neuroanatomical and functional changes that lead to cardiovascular impairment.

Parkinson's disease (PD) is associated with respiratory dysfunction. In the 6-OHDA rat model of PD this is seen as a reduction in respiratory frequency and minute ventilation during normoxia and hypercapnia stimulus. r Respiratory dysfunction is caused by neuronal death of medullary respiratory nuclei in the 6-OHDA model of PD. r Oxidative stress can be considered a strong candidate for neurodegeneration via miR-34c downregulation and pro-apoptotic signalling in respiratory neurons, preceding the functional impairment observed in the 6-OHDA model of PD.

We showed recently that pressure fall in trained spontaneously hypertensive rats (SHR) is correlated with decreased vascular resistance and skeletal muscle wall/lumen ratio normalization without changes in renal arterioles (J. Hypertens. 18: 1563(J. Hypertens. 18: , 2000 Hypertension 42 [part 2]: 851, 2003). In the present study, we investigated the effects of physical training on sympathetic vascular innervation to different tissues and adrenal catecholamines (hormoral response).Male SHR (~2 months) were submitted to treadmill physical training (50-60% of maximal exercise capacity, 1 h/day, 5 d/weeks, 3 months) or kept sedentary (S), and then instrumented for pressure (AP) and heart rate (HR) recordings at rest. Rats were deeply anesthetized and tissues (soleus, gastrocnemius red, gracilis = locomotor; temporalis = non-locomotor muscle; kidney and adrenals) were collected for immunohistochemistry (PBS + PFA 4%, half of the rats in each group) and expression (Western Blot analysis) of tyrosine hydroxylase (TH).Physical training improved treadmill performance (+0.60±0.13 km/h), and reduced AP and HR at rest (177±3 mmHg and 319±7 b/mim, corresponding 6% and 10% fall vs S group, p<0.05). After physical training, TH immunoreactivity was increased in locomotor muscles (+57% on average, p<0.05) with smaller changes in the temporalis (+24%, p>0.05), without any change in kidney arterioles. Traininginduced TH imunorreactivity increase within the locomotor muscles was accompanied by significant reduction of arterioles wall/lumen ratio. There was no change on TH expression in the adrenals.