NE (levarterenol, l-noradrenaline) is released by mammalian postganglionic sympathetic nerves (Table 10-1). NE constitutes 10-20% of the catecholamine content of human adrenal medulla and as much as 97% in some pheochromocytomas, which may not express phenylethanolamine-N-methyltransferase.
PHARMACOLOGICAL PROPERTIES The pharmacological actions of NE and Epi have been extensively compared in vivo and in vitro (Table 10-2). They are approximately equipotent in stimulating b1 receptors; they differ mainly in their effectiveness in stimulating a and b2 receptors. NE is a potent a agonist and has relatively little action on b2 receptors; however, it is somewhat less potent than Epi on the a receptors of most organs. Isoproterenol stimulates all b receptors but not a receptors. Figure 10-2 compares the cardiovascular effects of infusions of NE, Epi, and isoproterenol.
Cardiovascular Effects In response to infused NE, systolic and diastolic pressures, and usually pulse pressure, increase (see Figure 10-2). Cardiac output is unchanged or decreased, and total peripheral resistance is raised. Compensatory vagal reflex activity slows the heart, overcoming direct cardioaccelerator action; stroke volume increases. Peripheral vascular resistance increases in most vascular beds, and renal blood flow is reduced. NE constricts mesenteric vessels and reduces splanchnic and hepatic blood flow. Coronary flow usually is increased, probably owing both to indirectly induced coronary dilation, as with Epi, and to elevated blood pressure. Although generally a poor b2 agonist, NE may increase coronary blood flow directly by stimulating b2 receptors on coronary vessels. Patients with Prinzmetal's variant angina may be supersensitive to the a constrictor effects of NE.
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