title: Ankle oedema and sympathetic activation.
abstract: Ankle oedema is a common adverse event during treatment with dihydropyridine (DHP) calcium channel antagonist therapy, the incidence of which is dose related. The three mechanisms put forward to explain the formation of oedema during calcium channel antagonist therapy are arteriolar vasodilation, impairment of the local vascular autoregulation of blood flow and impaired protection against hydrostatic load. The importance of differential arteriolar-venular dilation has been demonstrated in numerous clinical studies. In particular, differences in sympathetic overactivation after arterial vasodilation have been shown to be related to differences in ankle oedema rates. If these results are confirmed, calcium channel antagonists that activate the sympathetic nervous system to a lesser extent, such as manidipine, may become first-choice calcium channel antagonists because of their more favourable adverse event profile.
authors.affiliation: Department of Internal Medicine, University of Pavia, Pavia, Italy. r.fogari@smatteo.pv.it
authors.forename: Roberto
authors.initials: R
authors.lastname: Fogari
mesh_terms: D000843:Ankle Joint; D001160:Arterioles / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000009:adverse effects*; D004095:Dihydropyridines / Q000009:adverse effects*; D004487:Edema / Q000139:chemically induced*; D006801:Humans; D007592:Joint Diseases / Q000139:chemically induced*; D009638:Norepinephrine / Q000378:metabolism; D016032:Randomized Controlled Trials as Topic; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000378:metabolism; D014664:Vasodilation
chemical_list: D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D009638:Norepinephrine