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Our research at the Freiburg Physiological Institute over the past
25 years has demonstrated that specific calcium antagonists
interfere with all physiological and pathophysiological reactions
involving the heart and vessels in which an elevated inflow of
calcium ions across the potential-dependent slow membrane channels
into the cells is a decisive factor. From the outset, our
therapeutic interest has centred on the possibility of inhibiting
excessively high levels of transmembrane cal- cium influx and
thereby reducing the pathogenic consequences of intra- cellular
calcium overload. For example, all excessive calcium influx evokes
contractile hyperactivity, which manifests itself in the myocardial
fibres as hyperkinetic reactions and an uneconomic rise in oxygen
de- mand and, analogously, in vascular smooth muscle cells as
increased tonus and spasm. The therapeutic use of calcium
antagonists to inhibit excessive mechanical and metabolic activity
in the myocardium and to achieve prophylaxis and lysis in smooth
muscle spasm was therefore a logical step. The highest potencies of
calcium antagonists were found in the vas- cular smooth musculature
(coronary, cerebral, mesenteric and renal arteries and other
systemic resistance vessels). Consequently, calcium antagonists
were recognized as the agents of choice for numerous indica- tions
for vascular therapy. It is well established that calcium ions are
also essential for the generation of impulses in cardiac pacemaker
cells and for the conduc- tion of electrical charges.
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