Overview of Modes of Action A

1. The pumping capacity of the heart is regulated by sympathetic and parasympathetic nerves (pp. 84, 105). Drugs capable of interfering with autonomic nervous function therefore provide a means of influencing cardiac performance. Thus, anxiolytics of the benzodiazepine type (p. 226), such as diaze-pam, can be employed in myocardial infarction to suppress sympathoactiva-tion due to life-threatening distress. Under the influence of antiadrenergic agents (p. 96), used to lower an elevated blood pressure, cardiac work is decreased. Ganglionic blockers (p. 108) are used in managing hypertensive emergencies. Parasympatholytics (p. 104) and p-blockers (p. 92) prevent the transmission of autonomic nerve impulses to heart muscle cells by blocking the respective receptors.

2. An isolated mammalian heart whose extrinsic nervous connections have been severed will beat spontaneously for hours if it is supplied with a nutrient medium via the aortic trunk and coronary arteries (Langendorff preparation). In such a preparation, only those drugs that act directly on cardio-myocytes will alter contractile force and beating rate.

Parasympathomimetics and sym-pathomimetics act at membrane receptors for visceromotor neurotrans-mitters. The plasmalemma also harbors the sites of action of cardiac glycosides (the Na/K-ATPases, p. 130), of Ca2+ antagonists (Ca2+ channels, p. 122), and of agents that block Na+ channels (local anesthetics; p. 134, p. 204). An intracel-lular site is the target for phosphodies-terase inhibitors (e.g., amrinone, p. 132).

3. Mention should also be made of the possibility of affecting cardiac function in angina pectoris (p. 306) or congestive heart failure (p. 132) by reducing venous return, peripheral resistance, or both, with the aid of vasodilators; and by reducing sympathetic drive applying p-blockers.

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