Pharmacology Answers-12

(C) The cardiac manifestations of beta-blocker
intoxication can be very severe, resulting in
bradycardia, AV blockade, and markedly
reduced force of contraction and cardiac
output. Hypotension is common. However, the
heart has glucagon receptors that are linked to
stimulation of adenylyl cyclase independent of
beta adrenoreceptors, which mediate marked
increases in rate and force and substitute for the
blocked beta response. (Glucagon also plays a
primary role in raising blood glucose levels
through activation of glycogenolysis and gluconeogenesis.)
Atrial natriuretic peptide (choice
A) is released from the cardiac atria and causes
vasodilation through activation of membranebound
guanylyl cyclase in arteriolar smooth
muscle, and sodium excretion in the urine
through an increase in glomerular filtration
rate and consequent increase in filtration fraction.
It is of no value in beta-blocker overdose.
If the beta-blocker overdose is sufficient,
administration of beta agonists such as epinephrine
(choice B) is inadequate to overcome
the blockade. Human growth hormone
(choice D) is a peptide hormone produced by
the anterior pituitary. It stimulates growth at
open epiphyses through production of the
insulin-like growth factors. It has no direct
effect on cardiac function. Insulin (choice E)
activates entry of glucose into most tissues and
promotes glycogen and triglyceride storage. It
has no direct effects on cardiac function.

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