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KEY CONCEPTS

KEY CONCEPTS

  • Image not available. Adrenergic agonists can be categorized as direct or indirect. Direct agonists bind to the receptor, whereas indirect agonists increase endogenous neurotransmitter activity.

  • Image not available. The primary effect of phenylephrine is peripheral vasoconstriction with a concomitant rise in systemic vascular resistance and arterial blood pressure.

  • Image not available. Clonidine decreases anesthetic and analgesic requirements and provides sedation and anxiolysis.

  • Image not available. Dexmedetomidine has a higher affinity for α2-receptors than clonidine. It has sedative, analgesic, and sympatholytic effects that blunt many of the cardiovascular responses seen during the perioperative period.

  • Image not available. Long-term use of these agents, particularly clonidine and dexmedetomidine, leads to super-sensitization and upregulation of receptors; with abrupt discontinuation of either drug, an acute withdrawal syndrome including hypertensive crisis can occur.

  • Image not available. Ephedrine is commonly used as a vasopressor during anesthesia. As such, its administration should be viewed as a temporizing measure while the cause of hypotension is determined and remedied.

  • Image not available. At low doses (0.5–3 mcg/kg/min), dopamine (DA) primarily activates dopaminergic receptors. Stimulation of these receptors (specifically, DA1 receptors) vasodilates the renal vasculature and promotes diuresis.

  • Image not available. Labetalol lowers blood pressure without reflex tachycardia because of its combination of α and β effects.

  • Image not available. Esmolol is an ultrashort-acting selective β1-antagonist that reduces heart rate and, to a lesser extent, blood pressure.

  • Image not available. Abrupt discontinuation of β-blocker therapy for 24 to 48 h may trigger a withdrawal syndrome characterized by hypertension, tachycardia, and angina pectoris.

Adrenergic agonists and antagonists produce their clinical effects by interacting with the adrenergic receptors (ie, adrenoceptors). The clinical effects of these drugs can be deduced from an understanding of the adrenoceptor physiology and a knowledge of which receptors each drug activates or blocks.

ADRENOCEPTOR PHYSIOLOGY

The term adrenergic originally referred to the effects of epinephrine (adrenaline), although norepinephrine (noradrenaline) is the primary neurotransmitter responsible for most of the adrenergic activity of the sympathetic nervous system. With the exception of eccrine sweat glands and some blood vessels, norepinephrine is released by postganglionic sympathetic fibers at end-organ tissues (Figure 14–1). In contrast, acetylcholine is released by preganglionic sympathetic fibers and all parasympathetic fibers.

FIGURE 14–1

The sympathetic nervous system. Organ innervation, receptor type, and response to stimulation. The origin of the sympathetic chain is the thoracoabdominal (T1–L3) spinal cord, in contrast to the craniosacral distribution of the parasympathetic nervous system. Another anatomic difference is the greater distance from the sympathetic ganglion to the visceral structures.

Norepinephrine is synthesized in the cytoplasm of sympathetic postganglionic nerve endings and stored in the vesicles (Figure 14–2). After release by a process of exocytosis, the action of norepinephrine is primarily terminated by reuptake into the postganglionic nerve ending. Norepinephrine transporter located on neuronal cell membranes facilitates removal of norepinephrine from the synapse. Other transporters facilitate uptake of dopamine and serotonin. Tricyclic antidepressants, cocaine, and amphetamines ...

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