Drugs affecting blood vessels

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Many different drugs and endogenous substances cause constriction or dilation of blood vessels. Drugs that have a direct relaxant effect on vascular smooth muscle include the organic nitrates (e.g., nitroglycerin tablets, which are mainly used to treat angina) and calcium antagonists (e.g., nifidipine). Most blood vessels are controlled by the sympathetic nervous system, and they constrict in response to norepinephrine released from sympathetic nerves. Thus, drugs that affect the sympathetic system cause constriction or dilation of blood vessels. The parasympathetic nervous system is much less important in controlling blood vessels.

Apart from the actions of the sympathetic nervous system, several other physiological mechanisms regulate vascular smooth muscle. Of particular pharmacological importance are the renin-angiotensin system and locally acting vasodilator substances, such as histamine, bradykinin, and prostaglandins.

Renin is an enzyme that is released into the bloodstream by the kidney when the blood pressure falls. It acts on a plasma protein to produce a peptide, angiotensin I, which consists of a chain of 10 amino acids. This in turn is acted on by angiotensin converting enzyme (ACE) to produce an eight-ammo acid peptide, angiotensin II (a potent vasoconstrictor), which raises the blood pressure. Inhibitors of ACE are used in treating high blood pressure.

Various substances that act on blood vessels are released when tissues are damaged by disease or injury. Histamine is stored by special cells in the skin and elsewhere, and when it is released histamine causes capillary walls to leak fluid, resulting in local tissue swelling. Prostaglandins and bradykinin have similar functions. All of these substances apparently act locally in the process of inflammation rather than systemically in overall cardiovascular regulation.

Inotropic agents are drugs that influence the force of contraction of cardiac muscle, thereby tending to affect the cardiac output. Drugs have a positive inotropic effect if they increase the force of contraction of the heart. The most important group of inotropic agents is the cardiac glycosides, substances that occur in the leaves of the foxglove (Digitalis purpurea) and other plants.

Although they have been used for many purposes throughout the centuries the effectiveness of cardiac glycosides in heart disease was established in 1785 by an English physician, William Withering who successfully used an extract of foxglove leaves to treat heart failure. Many closely related glycosides with similar pharmacological actions are found in various plants, but they differ in ease of absorption from the gastrointestinal tract and in duration of action. The two compounds most often used therapeutically are digoxin and digitoxin.

The most useful effect of cardiac glycosides is their ability to increase the force of contraction of cardiac muscle. They have, however, several additional effects, most of which are disadvantageous. These include a tendency to block conduction of the electrical impulse that causes contraction as it passes from the atria to the ventricles of the heart (heart block). Cardiac glycosides also have a tendency to produce an abnormal cardiac rhythm by causing electrical impulses to be generated at points in the heart other than the normal pacemaker region, the cells that rhythmically maintain the heartbeat These irregular impulses result in ectopic heartbeats that are out of sequence with the normal cardiac rhythm. Occasional ectopic beats are harmless, but if this process continues to a complete disorganization of the cardiac rhythm (ventricular fibrillation), the pumping action of the heart is stopped, causing death within minutes unless resuscitation is carried out. Because the margin of safety between the therapeutic and the toxic doses of glycosides is relatively narrow, they must be used carefully.

Cardiac glycosides are believed to increase the force of cardiac muscle contraction by binding to and inhibiting the action of a membrane enzyme that extrudes sodium ions from the cell interior. Inhibiting the free flow of sodium ions from the interior of the cell across the membrane to the exterior of the cell causes the intracellular sodium concentration to rise. The interior of the cell then becomes depolarized, or electrically less negative than normal with respect to the exterior of the cell. Because the cell is able to exchange sodium ions within the cell for calcium ions outside it, there is a secondary rise in intracellular calcium. This subsequently increases the force of contraction, since intracellular calcium ions are responsible for initiating the shortening of muscle cells.

The disturbances of rhythm that may be caused by cardiac glycosides result partly from the depolarization and partly from the increase in intracellular calcium. Because these rhythm disturbances are caused by the same underlying mechanism that causes the beneficial effect, there is no likelihood of finding a cardiac glycoside with a significantly better margin of safety. Apart from their cardiac actions, these glycosides tend to cause nausea and loss of appetite. Because digoxin and digitoxin have long plasma half-lives (two and seven days, respectively), they are liable to accumulate in me body. Treatment with either of these drugs must involve careful monitoring to avoid the adverse effects that may result from their slow buildup in the body.

The second type of inotropic agent that increases the force of cardiac muscle contraction includes epinephrine and norepinephrine. In addition to affecting the force of contraction, however, they also increase the heart rate. This, and the fact that they are quickly metabolized by the body and act only for a few minutes, means that they are not useful inotropic agents.

The third type of inotropic agent that acts as a cardiac stimulant is the caffeine-related series of drugs represented by theophylline.

The heart rate is controlled by the opposing actions of sympathetic and parasympathetic nerves and by the action of epinephrine released from the adrenal gland. Norepinephrine, released by sympathetic nerves in the heart, and epinephrine, released by the adrenal gland, increase the heart rate, while acetylcholine, released from parasympathetic nerves, decreases it. A competitive antagonist that acts to inhibit the stimulating action of norepinephrine on the heart is propranolol, which slows the heart and is often used to treat anginal attacks and disturbances of cardiac rhythm. Atropine blocks acetylcholine receptors and is used during anesthesia to prevent excessive cardiac slowing.