Arterial hypertension, a tricky side of Parkinson’s disease: physiopathology and therapeutic features

The role of arterial hypertension (HT) as risk factor for Parkinson’s disease (PD) is still debated. Case–control and retrospective studies do not support an association between HT and PD and the risk of PD seems to be lower in hypertensive than in normotensive subjects. In addition, the use of calcium-channel blockers (CCBs) and angiotensin-converting enzyme inhibitors seems to have a protective effect on the risk of developing PD. In clinical practice, a crucial finding in subjects with PD is the high supine systolic blood pressure (SBP) coupled with orthostatic hypotension (OH). It is not clear whether this SBP load could be a risk factor for target organ damage as this load can be largely due to the drugs used to treat OH (i.e., fludrocortisone acetate, midodrine) or PD itself (i.e., monoamine oxidase inhibitors, dopamine D2-receptor antagonists). This blood pressure (BP) load is largely independent of medications as the 40 % of subjects with PD have a non-dipping pattern of BP during 24 h ambulatory monitoring (24-h ABPM). In PD, nocturnal HT is usually asymptomatic and 24-h ABPM should be used to track both supine HT and OH. Treatment of HT in PD is difficult because the reduction of supine BP could worsen OH. To avoid this, short-acting dihydropyridine CCBs, clonidine or nitrates are recommended, assuming between meals, in late afternoon or in the evening in avoiding an aggravation in the post-prandial hypotension characteristic of PD.