Calcium Entry Blockers in Cardiovascular and Cerebral Dysfunctions
[Book]
edited by Théophile Godfraind, Arnold G. Herman, Donald Wellens.
Dordrecht
Springer Netherlands
1984
(325 pages)
Developments in cardiovascular medicine, 40.
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.
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).
Cardiology.
Medicine.
RC684
.
C34
E358
1984
edited by Théophile Godfraind, Arnold G. Herman, Donald Wellens.