The prevalence of orthostatic hypotension (OH) in hypertensive patients ranges from 3 to 26%. Drugs are a common cause of non-neurogenic OH. In the present study, we retrospectively evaluated the medical records of 9242 patients with essential hypertension referred to our Hypertension Unit. We analysed data on supine and standing blood pressure values, age, sex, severity of hypertension and therapeutic associations of drugs, commonly used in the treatment of hypertension. OH was present in 957 patients (10.4%). Drug combinations including α-blockers, centrally acting drugs, non-dihydropyridine calcium-channel blockers and diuretics were associated with OH. These pharmacological associations must be administered with caution, especially in hypertensive patients at high risk of OH (elderly or with severe and uncontrolled hypertension). Angiotensin-receptor blocker (ARB) seems to be not related with OH and may have a potential protective effect on the development of OH.

Reverse nocturnal blood pressure dipping is a marker of cardiovascular dysautonomia in Parkinson disease, which can be screened for with ease and affordability using ambulatory blood pressure monitoring.

disease (PD): its prevalence ranges between 14% and 80% [12]. It is related to older age, severity and duration of the disease [13,14] and can be caused by autonomic dysfunction, drugs, or both causes. Few studies have evaluated the specific mechanisms of orthostatic hypotension in patients with PD. Lowering of blood pressure may be mainly due to drugs (in particular levodopa), when autonomic cardiovascular function tests are normal [15]. On the other hand, the absence of activation of compensatory chronotropic mechanisms to low blood pressure while standing may be due to autonomic failure [16]. Dopaminergic agonists (levodopa, carbidopa) frequently cause orthostatic hypotension, even at the beginning of therapy, through the activation of dopamine receptors, determining cutaneous, mesenteric and renal vasodilation, but also through other mechanisms, such as a reduced central sympathetic tone, which causes a small reduction in heart rate, and an impaired release of renin and aldosterone [17,18]. However, among antiparkinsonian drugs, selegiline seems to be more frequently involved in the onset of orthostatic hypotension, even after long-term therapy, if compared to levodopa [16,19]. Furthermore, while combined treatment with both drugs can determine severe orthostatic hypotension [20,21], levodopa alone is less often responsible for this phenomen. In fact, in additon to the peripheral vasodilatation due to dopamine agonists, the decreased reuptake of dopamine and norepinephrine in central neurvous system caused by selegiline causes a reduction in sympathetic tone [22]. Ha et al. [13] did not find a significant difference in dopaminergic agonist doses between PD patients with and without symptoms related to orthostatic hypotension, suggesting that other factors, such as age and other concomitant therapies, may be responsible for orthostatic hypotension in PD [13]. These data were further confirmed by Perez-Lloret et al.

Autonomic failure (AF) is characterized by orthostatic hypotension, supine hypertension, and increased blood pressure (BP) variability. AF patients develop cardiac organ damage, similarly to essential hypertension (EH), and have higher arterial stiffness than healthy controls. Determinants of cardiovascular organ damage in AF are not well known: both BP variability and mean BP values may be involved. The aim of the study was to evaluate cardiac organ damage, arterial stiffness, and central hemodynamics in AF, compared with EH subjects with similar 24-hour BP and a group of healthy controls, and to evaluate determinants of target organ damage in patients with AF. Twenty-seven patients with primary AF were studied (mean age, 65.7±11.2 years) using transthoracic echocardiography, carotid-femoral pulse wave velocity, central hemodynamics, and 24-hour ambulatory BP monitoring. They were compared with 27 EH subjects matched for age, sex, and 24-hour mean BP and with 27 healthy controls. AF and EH had similar left ventricular mass (101.6±33.3 versus 97.7±28.1 g/m 2 , P =0.59) and carotid–femoral pulse wave velocity (9.3±1.8 versus 9.2±3.0 m/s, P =0.93); both parameters were significantly lower in healthy controls ( P <0.01). Compared with EH, AF patients had higher augmentation index (31.0±7.6% versus 26.1±9.2%, P =0.04) and central BP values. Nighttime systolic BP and 24-hour systolic BP predicted organ damage, independent of BP variability. AF patients develop hypertensive heart disease and increased arterial stiffness, similar to EH with comparable mean BP values. Twenty-four–hour and nighttime systolic BP were determinants of cardiovascular damage, independent of BP variability.

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