Adrenergics Module: Answers to Self Assessment Questions

A patient with hyperparathyroidism has increased serum calcium levels. Observation of the patient's electrocardiogram could show:

  • Lengthened R-R interval
  • Lengthened Q-T interval 
  • Presence of a J-wave
  • Both lengthened Q-T interval and the presence of a J-wave 

Hypercalcemia results in a shortening of the Q-T interval. A J-wave may also be present (along with a shortened Q-T interval). Heart rate is not generally altered unless hypercalcemia is very severe, and if there are changes heart rate would increase (the R-R interval is shortened).

A moderate dose of dopamine:

  • Produces a positive chronotropic effect with little inotropic effect 
  • Produces a large increase in total peripheral resistance 
  • Acts as a sympatholytic 
  • Produces a positive inotropic effect with little chronotropic effect

Moderate doses of dopamine activate D1 receptors in the kidney as well as β-1 receptors. Moderate doses of dopamine produce a selective increase in the force of myocardial contraction without a significant effect on heart rate. Thus, there is a modest decrease in total peripheral resistance (due to renal vasodilation), a positive inotropic effect, but little chronotropic effect. Since the drug activates β-1 receptors, it would be classified as a sympathomimetic.

Binding of agonist to which of the following receptors activates phospholipase C?

  • Alpha-1
  • Alpha-2
  • Beta-1
  • Beta-2

Binding of agonist to an α-1 receptor activates phospholipase C. Binding of agonist to other adrenergic receptors affects cAMP.

Clonidine:

  • Raises blood pressure by causing an increase in norepinephrine release from sympathetic efferent fibers 
  • Lowers blood pressure by activating presynaptic alpha-2 receptors in the brain
  • Raises blood pressure by increasing the activity of RVLM neurons
  • Lowers blood pressure by blocking presynaptic alpha-2 receptors in the brain

Clonidine is an α-2 receptor agonist, which selectively activates α-2 receptors in the brainstem. This causes a decrease in the activity of RVLM neurons, resulting in reduced sympathetic nervous system activity and lowered blood pressure.

Which of the following drugs produces a marked DECREASE in total peripheral resistance?

  • Norepinephrine 
  • High dose of dopamine 
  • Low dose of dobutamine 
  • Prazosin 

Prazosin is an  α-1 receptor antagonist, and thus causes widespread vasodilation and reduced total peripheral resistance. Norepinephrine and high doses of dopamine are α-1 receptor agonists, and thus INCREASE total peripheral resistance. A low dose of dobutamine is a β-1 agonist, and does not directly affect the vasculature. However, dobutamine raises blood pressure, and could cause a baroreceptor reflex-mediated decrease in total peripheral resistance. However, the effect would not be a drastic as that produced by Prazosin.

Which of the following drugs produces the largest INCREASE in total peripheral resistance?

  • Norepinephrine
  • Epinephrine
  • Dopamine--small dose 
  • Phentolamine

Norepinephrine produces large increases in total peripheral resistance by acting on α-1 receptors. Epinephrine also binds to β-2 receptors, causing simultaneous vasodilation and vasoconstriction, and thus moderate changes in total peripheral resistance. Small doses of dopamine increase renal blood flow, thus lowering total peripheral resistance. Phentolamine is an α-receptor antagonist, and thus lowers total peripheral resistance.

Administration of a selective beta-2 agonist would produce:

  • Vasodilation and a reflex-mediated positive inotropic effect
  • Less norepinephrine release from sympathetic efferent fibers in the heart
  • Vasoconstriction and a reflex-mediated negative inotropic effect
  • Vasodilation without any effects on the heart

β-2 agonists cause vasodilation of muscle arterioles, thereby lowering total peripheral resistance and blood pressure. As a result, there is a baroreceptor-mediated increase in both heart rate and contractility.

Which of the following drugs DECREASES myocardial oxygen demand?

  • Isoproterenol
  • Prazosin
  • Beta-1 receptor antagonist
  • Dopamine--high dose

Isoproterenol and high doses of dopamine directly produce positive chronotropic and inotropic effects, thereby increasing myocardial oxygen demand. Prazosin produces vasodilation, and thus baroreceptor-mediated positive chronotropic and inotropic effects. In contrast a β-1 receptor antagonist blocks sympathetic effects on the heart, causing negative chronotropic and inotropic effects.

A selective antagonist for ganglionic nicotinic receptors like Trimetaphan:

  • Increases both sympathetic and parasympathetic postganglionic activity
  • Depresses epinephrine release into the bloodstream
  • Decreases sympathetic efferent activity, but has no effect on the parasympathetic system
  • Decreases parasympathetic efferent activity, but has no effect on the sympathetic system

Trimetaphan would block nicotinic receptors on both sympathetic and parasympathetic postganglionic neurons, suppressing activity of both parasympathetic and sympathetic efferent fibers. It also would depress epinephrine release from the adrenal medulla, as medullary chromaffin cells have the same receptors as sympathetic postganglionic neurons.