The sympathetic nervous system, @entity453 and @entity296 are related in different ways. First, the sympathetic system may be involved in the process of @entity731 through platelet activation and subsequent platelet-derived growth factor formation and by inducing mechanical injury to the vascular wall as a result of increased blood pressure and increased flow velocity. Secondly, sympathetic control of coronary vasomotor tone, which under normal conditions is not important, becomes functionally significant once @entity453 has occurred. Under these circumstances, increased sympathetic adrenergic tone may lead to coronary vasoconstriction and, as myocardial @entity26 demand increases concomitantly, @entity296 may ensue. Alternatively, @entity296 activates several neurohormonal systems, such as the sympathetic and, during more severe ischaemia, the circulating renin-angiotensin system. This leads to systemic and, possibly, coronary vasoconstriction and thus to further @entity296 . Prolonged @entity296 results in progressive @entity1063 release from the heart, reaching extracellular levels as high as 100-1000 x plasma concentrations. As cardiac beta-receptor density rises simultaneously, sympathetically-induced irreversible @entity296 may occur, although through concomitantly increased beta-receptor kinase activity the beta-receptor may become functionally inactive. To counteract the detrimental effects of enhanced sympathetic activation on the heart, beta-blockade appears to be the proper choice. However, acute beta-blockade may lead to more profound ischaemia-induced neurohormonal activation and hence to vascular constriction through unoccupied alpha-receptors. In contrast, under ischaemic conditions and with concomitant beta-blockade, acute alpha-blockade does improve subendocardial flow and reduces @entity296 . A novel approach to anti-ischaemic therapy, which relates to modulating ischaemia-induced sympathetic activation, is through @entity1289 inhibition. @entity1289 inhibitors affect @entity296 by reducing neurohormonal activation and related systemic and coronary vasoconstriction. These acute effects may become more important over time, as coronary endothelial function improves following long-term @entity1289 inhibition. A large multicentre controlled trial comparing @entity1289 inhibition with placebo in @entity1 with @entity453 , the EUROPA (EUopean trial on Reduction Of @entity299 with Perindopril in stable @entity453 ), which is currently underway, addresses the issue of whether @entity1289 inhibition does in fact offer a novel approach in @entity296 .

The sympathetic nervous system and XXXX .

@entity1 :: ('9606', 'Species') :: ['patients'] @entity296 :: ('MESH:D009202', 'Disease') :: ['myocardial ischaemia', 'myocardial damage'] @entity1289 :: ('1636', 'Gene') :: ['ACE'] @entity731 :: ('MESH:D050197', 'Disease') :: ['atherosclerosis'] @entity26 :: ('MESH:D010100', 'Chemical') :: ['oxygen'] @entity299 :: ('MESH:D006331', 'Disease') :: ['cardiac events'] @entity453 :: ('MESH:D003324', 'Disease') :: ['coronary artery disease endothelial dysfunction', 'coronary Artery disease', 'coronary artery disease'] @entity1063 :: ('MESH:D009638', 'Chemical') :: ['norepinephrine']
@entity299 :: (MESH:D006331,Disease) :: ['ischaemic heart disease']
