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Abbreviations: Epi, epinephrine; NE, norepinephrine; +, increase; 0, no change; -, decrease; after atropine, +.

vascular reactivity as a result of tissue hypoxia rather than to b agonist activity of the drug on mucosal vessels.

Blood flow to skeletal muscles is increased by therapeutic doses, due in part to powerful b2-mediated vasodilation that is only partially counterbalanced by vasoconstrictor via the a receptors that also are present. If an a receptor antagonist is given, vasodilation in muscle is more pronounced, total peripheral resistance is decreased, and mean blood pressure falls (Epi reversal). After the administration of a nonselective b receptor antagonist, Epi produces only vasoconstriction and a considerable pressor effect.

In usual therapeutic doses, Epi has little constrictor action on cerebral arterioles. The cerebral circulation does not constrict in response to activation of the sympathetic nervous system by stressful stimuli; indeed, autoregulatory mechanisms tend to limit the increase in cerebral blood flow caused by increased blood pressure.

Doses of Epi that have little effect on mean arterial pressure consistently increase renal vascular resistance and reduce renal blood flow. All segments of the renal vascular bed contribute to the increased resistance. Since the glomerular filtration rate is only slightly and variably altered, the filtration fraction is consistently increased. Excretion of Na+, K+, and Cl- is decreased. Maximal tubular reabsorptive and excretory capacities are unchanged. The secretion of renin is increased as a consequence of the stimulation of bj receptors on the juxtaglomerular cells (see Figure 30-2).

Epi increases arterial and venous pulmonary pressures. Although direct pulmonary vasoconstriction occurs, redistribution of blood from the systemic to the pulmonary circulation, due to constriction of the more powerful musculature in the systemic great veins, contributes to an increase in pulmonary pressure. Very high concentrations of Epi may cause pulmonary edema precipitated by elevated pulmonary capillary filtration pressure and possibly by "leaky" capillaries.

Coronary blood flow is enhanced by Epi or by cardiac sympathetic stimulation under physiological conditions. The increased flow, which occurs even with doses that do not increase the aortic blood pressure, is the result of two factors. The first is the increased relative duration of diastole at higher heart rates (see below); this is partially offset by decreased blood flow during systole because of more forceful contraction of the surrounding myocardium and an increase in mechanical compression of the coronary vessels. The increased flow during diastole is further enhanced if aortic blood pressure is elevated by Epi; as a consequence, total coronary flow may be increased. The second factor is a metabolic dilator effect that results from the increased strength of contraction and myocardial O2 consumption due to direct effects of Epi on cardiac myocytes. This vasodilation is mediated in part by adenosine released from cardiac myocytes, which tends to override a direct vasoconstrictor effect of Epi that results from activation of a receptors in coronary vessels.

CARDIAC EFFECTS Epi is a powerful cardiac stimulant. Direct responses to Epi include increase in the rate of tension development, peak contractile force, and rate of relaxation; decreased time to peak tension; increased excitability, acceleration of the rate of spontaneous beating, and induction of automaticity in specialized regions of the heart. Epi acts directly on the predominant b1 receptors of the myocytes and of the cells of the pacemaker and conducting tissues. The heart rate increases, and the rhythm often is altered. Cardiac systole is shorter and more powerful, cardiac output is enhanced, and the work of the heart and its O2 consumption are markedly increased. Cardiac efficiency (work done relative to O2 consumption) is lessened.

By increasing the rates of ventricular contraction and relaxation, Epi preferentially shortens systole and usually does not reduce the duration of diastole. Epi speeds the heart by accelerating the slow depolarization of sinoatrial (SA) nodal cells that takes place during phase 4 of the action potential (see Chapter 34). The amplitude of the AP and the maximal rate of depolarization (phase 0) also are increased. A shift in the location of the pacemaker within the SA node often occurs, owing to activation of latent pacemaker cells. In Purkinje fibers, Epi accelerates diastolic depolarization and may activate latent pacemakers. If large doses of Epi are given, premature ventricular contractions occur and may herald more serious ventricular arrhythmias. Conduction through the Purkinje system depends on the level of membrane potential at the time of excitation. Epi often increases the membrane potential and improves conduction in Purkinje fibers that have been excessively depolarized.

Epi normally shortens the refractory period of the atrioventricular (AV) node by direct effects on the heart, although doses of Epi that elicit a vagal reflex may indirectly slow the heart and prolong the AV node's refractory period. Epi decreases the grade of AV block that occurs as a result of disease, drugs, or vagal stimulation. Supraventricular arrhythmias may occur from the combination of Epi and cholinergic stimulation. Depression of sinus rate and AV conduction by vagal discharge probably plays a part in Epi-induced ventricular arrhythmias, since various drugs that block the vagal effect confer some protection. The actions of Epi in enhancing cardiac automaticity and in causing arrhythmias are effectively antagonized by b receptor antagonists. However, activation of cardiac a1 receptors prolongs the refractory period and strengthens myocardial contractions. Cardiac arrhythmias have been seen in patients after inadvertent intravenous administration of conventional subcutaneous doses of Epi.

Epi and other catecholamines may cause myocardial cell death, particularly after intravenous infusions. Acute toxicity is associated with contraction band necrosis and other pathological changes; prolonged sympathetic stimulation of the heart, such as in congestive cardiomyopathy, may promote apoptosis of cardiomyocytes.

NONVASCULAR SMOOTH MUSCLES The effects of Epi on smooth muscle depend on the types and densities of adrenergic receptors expressed by the muscle (see Table 6-1). In general, Epi relaxes GI smooth muscle, due to activation of both a and b receptors. Intestinal tone and the frequency and amplitude of spontaneous contractions are reduced. The stomach usually is relaxed. By contrast, the pyloric and ileocecal sphincters are contracted (but these effects depend on the preexisting tone of the muscle; if tone already is high, Epi causes relaxation; if low, contraction).

The responses of uterine muscle to Epi vary with phase of the sexual cycle, state of gestation, and dose. During the last month of pregnancy and at parturition, Epi inhibits uterine tone and contractions. b2-Selective agonists (e.g., ritodrine or terbutaline) can delay premature labor, although their efficacy is limited (see below). Epi relaxes the detrusor muscle of the bladder (via activation of b receptors) and contracts the trigone and sphincter muscles (via a agonist activity). This can result in hesitancy in urination and may contribute to retention of urine in the bladder. Activation of smooth muscle contraction in the prostate promotes urinary retention.

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