“…Considering that OH can occur also as a complication of antiparkinsonian therapy, in the last decades many studies have been performed to test cardiovascular effects of different DAs on PD patients. Ergot DA, acting on both D1 and D2 dopamine receptors, induced hypotension probably by decreasing noradrenergic tone [5,6], whereas non-ergot DA seemed to be less active on the cardiovascular system, probably because of selective binding to D2 dopamine receptors [24,25,26]. Nevertheless, acute OH has been reported after starting non-ergot DA therapy [27], and asymptomatic OH has also been largely noted as a common adverse event of non-ergot DA long-term treatment or prolonged-release formulations [28,29,30].…”