- Adrenergic agonists can be categorized as
direct or indirect. Direct agonists bind to the receptor, whereas
indirect agonists increase endogenous neurotransmitter activity.
- The primary effect of phenylephrine is peripheral
vasoconstriction with a concomitant rise in systemic vascular resistance
and arterial blood pressure.
- Clonidine appears to decrease anesthetic and
analgesic requirements and to provide sedation and anxiolysis.
- Dexmedetomidine is a novel lipophylic α-methylol
derivative with 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
- Long-term use of these agents, particularly clonidine
and dexmedetomidine, leads to supersensitization and up-regulation
of receptors; with abrupt discontinuation of either drug, an acute
withdrawal syndrome manifested by a hypertensive crisis can occur.
- 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.
- Small doses (≤ 2 μg/kg/min)
of dopamine (DA) have minimal adrenergic effects but activate dopaminergic
receptors. Stimulation of these nonadrenergic receptors (specifically,
DA1 receptors) vasodilates the renal vasculature and promotes
- Favorable effects on myocardial oxygen balance
make dobutamine a good choice for patients with the combination
of congestive heart failure and coronary artery disease, particularly
if peripheral vascular resistance and heart rate are already elevated.
- Labetalol lowers blood pressure without reflex
tachycardia because of its combination of α- and β-effects.
- Esmolol is an ultrashort-acting selective β1-antagonist
that reduces heart rate and, to a lesser extent, blood pressure.
- Discontinuation of β-blocker
therapy for 24–48 h may trigger a withdrawal syndrome characterized
by hypertension, tachycardia, and angina pectoris.
The three previous chapters presented the pharmacology of drugs
that affect cholinergic activity. This chapter introduces an analogous
group of agents that interacts at adrenergic receptors—adrenoceptors.
The clinical effects of these drugs can be deduced from an understanding
of adrenoceptor physiology
and a knowledge of which receptors each drug activates or blocks.
The term adrenergic originally referred to the effects of epinephrine
(adrenaline), as opposed to the cholinergic
effects of acetylcholine. It is now
known that norepinephrine (noradrenaline) is the 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 12–1). In contrast, as was
explained in Chapter 10, acetylcholine is
released by preganglionic sympathetic fibers and all parasympathetic
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 ...