Blockade of cardiac beta-1 receptors causes a decrease in heart rate, myocardial contractility, and velocity of cardiac contraction. Beta-blockers cause the heart muscle to work less, thus requiring less oxygen; in time of oxygen lack, such as during a heart attack or severe angina, this action can be life-saving. Because of the reduction in the oxygen requirement of the heart muscle, the beta-blocking drugs are effective in preventing the chest pain of angina pectoris. Because patients with angina have a high risk of devel¬oping a heart attack over ensuing years, beta-blockers are important for both pain and prevention.
An increase in adrenaline such as that produced during stress or vigorous exercise causes an increase in (1) the number and stickiness of blood platelets, (2) clotting factor VIII (the hemophilic factor), and (3) the viscosity of the blood. Beta-blockers block some harmful effects of adrenaline.
Beta-blockers have antiarrhythmic effects; they depress phase 4 diastolic depolarization and are effective in abolishing arrhythmias caused by increased catechol-amines. This action is particularly important in patients with ischemic heart disease. The electrical impulse traffic through the AV node in reduced with beta-blockers and the rate of conduction is slowed. This important action slows the heart rate in patients with rapid heart rates caused by atrial fibrillation. There is also a favorable effect on ventricular arrhythmias, particularly those induced by increased sympathetic activity observed in patients with oxygen lack to the myocardium because of obstructive coronary artery disease. Blockade of beta-1 receptors reduces activity of the renin–angiotensin system in the kidney by reducing renin released from the juxtaglomer-ular cells; this action causes some lowering of blood pressure.

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