Supplemental Reading

Burnstock G and Griffith SG. Nonadrenergic Innervation of Blood Vessels. Boca Raton, FL: CRC, 1988.

Gootman PM (ed.). Developmental Neurobiology of the Autonomic Nervous System. Clifton, NJ: Humana, 1986.

Insel PA and Feldman RD. ß-Adrenergic Receptors in Health and Disease. Boca Raton, FL: CRC, 1994.

Lee TJF. Endothelial messengers and cerebral vascular tone regulation. In: Olesen J and Edvinsson L (eds.). Headache Pathogenesis: Monoamines, Neuropeptides, Purines, and Nitric Oxide. Philadelphia: Lippincott-Raven, 1997:61-72.

Limbird E (ed.). The Alpha-2 Adrenergic Receptors. Clifton, NJ: Humana, 1988.

Missale C et al. Dopamine receptors: From structure to function. Physiol Rev 1998;78:189-225.

Moncada SR, Palmer MJ, and Higgs EA. Nitric oxide: Physiology, pathophysiology, and pharmacology. Pharmacol Rev 1991;43:109-142.

Patel TB et al. Molecular biological approaches to unravel adenylyl cyclase signaling and function. Gene 2001;16:13-25.

Post SR, Hammond HR, and Insel PA. Beta-adrenergic receptors and receptor signaling in heart failure. Annu Rev Pharmacol Toxicol 1999;39:343-360.

Case Study Help for the Heart

T. L. is a highly successful scientist who spends long hours in the laboratory and is constantly in demand as a speaker and reviewer for scientific papers and grants. He has a family history of cardiovascular disease, having lost both his father and grandfather before either reached age 60. He has recently noticed decreased energy, especially during exercise, and had symptoms (difficulty in breathing, chest pain) that took him to the emergency department. The examining physician thought the best treatment would be short-term therapy with a directly acting inotropic agent, especially one that would not markedly increase an already elevated heart rate. Based on a knowledge of the distribution of cardiovascular autonomic receptors, which of the following agents— epinephrine, norepinephrine, amphetamine, or dobutamine—would be a logical choice to use in this initial short-term treatment?

Answer: Dobutamine injection would provide particular benefit in meeting the therapeutic needs of this patient. Dobutamine augments ventricular contractility and thus enhances cardiac output, especially stroke volume, in patients with depressed cardiac function. It does this by stimulating p-adrenoceptors in the heart while producing relatively little increase in chronotropic activity or any significant elevation in systemic blood pressure since it lacks a-adrenoceptor stimulating effects. Thus, in contrast to a nonselective p-adrenoceptor stimulant such as isoproterenol, which increases cardiac output primarily by increasing heart rate, dobutamine's actions increase cardiac output without being accompanied by either a marked increase in heart rate or a significant increase in systemic vascular resistance.

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