Buch, Englisch, Band 40, 325 Seiten, Gewicht: 700 g
Buch, Englisch, Band 40, 325 Seiten, Gewicht: 700 g
Reihe: Developments in Cardiovascular Medicine
ISBN: 978-0-89838-658-5
Verlag: Springer
2 The free internal Ca+ concentration in human red cells is set according to the leak 2 and-pump principle: There is a finite passive Ca+ influx at the physiological 2 2 Ca+ -gradient across the membrane which is compensated by Ca+ pumping in the outward direction with a rate given by the degree of saturation of the A TP-fuelled Ca 2 pump at the steady-state internal Ca+ concentration. Simons (1982) recently devised a method allowing the measurement of the steady 2 2 state internal Ca+ concentration. Cells are suspended in media of different Ca+ con 2 2 tent whose Ca+ concentration is monitored by a Ca+ -selective electrode. When the cells are lysed (by digitonin) there is an upward or downward deflection of the elec 2 trode signal. At the point of zero deflection, the cellular Ca+ concentration equals that 2 of the medium. The result is, that in fresh human red blood cells the Ca+ concentra tion is; O.4,uM (this is an upper estimate; the true value may be considerably lower).
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Weitere Infos & Material
I: Introductory considerations.- The major steps in the discovery of calcium entry blockers.- Basic mechanisms and classification of calcium entry blockers.- Calcium entry blockers: perspectives.- Twenty-seven calcium entry blockers in development: a new chapter in pharmacology.- II: Calcium entry blockers and peripheral circulatory function.- Calcium-ions and excitation contraction coupling in vascular smooth muscle cells.- Laser microprobe mass analysis (LAMMA) as a technique to quantitate Ca2+ ions.- Vascular pharmacology of calcium entry blockers.- Calcium homeostasis in human red blood cells.- Impact of Ca2+ entry blockers on Ca2+ dependent mechanisms in red blood cells, platelets and endothelial cells.- Red blood cell microrheology and calcium antagonists.- Calcium e ntry blockers in the treatment of peripheral obliterative arterial disease.- III: Calcium entry blockers and myocardial function.- Pharmacology of calcium entry blockers in animal and human coronary arteries.- Calcium paradox and calcium entry blockers.- Myocardial oxygen deprivation and calcium deprivation: ultrastructural characteristics and clinical significance.- Basic and clinical aspects of myocardial protection by calcium entry blockers.- Effect of calcium entry blockers on impaired left ventricular wall motion.- The influence of Ca2+ entry blockers on hemodynamics and coronary blood flow, and its importance for the treatment of angina pectoris.- The use of selective calcium antagonism in variant (vasospastic) and classical (effort) angina pectoris.- Calcium entry blockers in cardiovascular therapy. Influence of diltiazem on hemodynamics and coronary blood flow.- IV: Calcium entry blockers and cerebral function.- Calcium entry blockers and cerebral function: an introduction.- Calcium entry blockers and cerebral resuscitation.- Effect of calcium entry blockers in models of brain hypoxia.- Calcium entry blockers in the therapy of vertebrobasilar insufficiency.- Calcium entry blockers and pharmacological aspects of migraine.- Clinical evaluation of calcium entry blockers in migraine.- V: Calcium entry blockers in hypertension treatment.- Double-blind comparison of the antihypertensive effects of verapamil and nifedipine.- Treatment of hypertension emergencies and chronic arterial hypertension with calcium entry blockers.- The effect of nifedipine on arterial pressure and reflex cardiac control.- Concluding remarks.- Why are Ca2+ entry blockers effective in the treatment of hypertension and tissue hypoxia?.- List of authors and co-authors.
