Question

After being stung by a bee, a child is given an intramuscular injection of epinephrine. Which action would lead to bronchodilation? (A) increased cAMP levels (B) increased cyclic guanosine monophosphate (cGMP) levels (C) increased IP3 levels (D) calcium influx (E) sequestration of calcium

Short answer

Option A: increased cAMP levels.

Step-by-step solution

Understand the Mechanism of Bronchodilation

Bronchodilation is the widening of the bronchi and bronchioles in the respiratory tract. Epinephrine triggers beta-2 adrenergic receptors, which are part of a signaling pathway that leads to relaxation of bronchial smooth muscles.

Recognize the Role of cAMP

The binding of epinephrine to beta-2 adrenergic receptors increases cyclic adenosine monophosphate (cAMP) in the smooth muscle cells. Elevated cAMP levels lead to the relaxation of the smooth muscle, causing bronchodilation.

Evaluate Other Options

- Increased cyclic guanosine monophosphate (cGMP) levels often lead to vasodilation but are not primarily involved in bronchodilation. - Increased IP3 levels lead to release of calcium from intracellular stores, generally causing smooth muscle contraction, not relaxation. - Calcium influx usually stimulates muscle contraction. - Sequestration of calcium reduces muscle contraction, but is not the primary mediator in bronchodilation via epinephrine.

Identify Correct Option

Based on the understanding that epinephrine causes bronchodilation by increasing cAMP levels through beta-2 adrenergic receptor activation, the correct action that leads to bronchodilation is Option A: increased cAMP levels.

Key concepts

Epinephrine and Bronchodilation

Epinephrine plays a vital role in the body's response to stress and emergency situations, such as allergic reactions. When a child experiences an allergic reaction, as indicated by a bee sting, epinephrine is often administered. This powerful hormone and neurotransmitter acts on the respiratory system to promote bronchodilation, which is the widening of the air passages in the lungs.
This process is essential for increasing airflow and improving breathing efficiency, helping to alleviate symptoms of an asthma attack or an allergic reaction.

• Epinephrine works its magic by binding to specific receptors in the bronchi, stimulating a cascade of intracellular events.
• These events ultimately result in the relaxation of the smooth muscle tissue within the airways.

The connection between epinephrine and bronchodilation revolves around a sophisticated signaling pathway involving beta-2 adrenergic receptors, which we'll delve into in the next section.

Beta-2 Adrenergic Receptors

Beta-2 adrenergic receptors are key players in the body's response to epinephrine, particularly in the context of bronchodilation. These receptors are located on the surface of smooth muscle cells in the respiratory tract. When epinephrine binds to these receptors, it activates a specific intracellular signaling mechanism.
This binding is crucial because it initiates a series of events that lead to the production of cyclic adenosine monophosphate (cAMP), a molecule that plays an essential role in the relaxation process.

• Once activated, these receptors trigger the production of cAMP within the cell.
• This leads to a reduction in calcium ion levels, crucial for muscle contraction.
• The decrease in calcium facilitates muscle relaxation, leading to bronchodilation.

Understanding the role of beta-2 adrenergic receptors aids in comprehending how bronchodilators, like epinephrine, can effectively relieve breathing difficulties during an asthma attack or allergic reaction.

cAMP in Smooth Muscle Relaxation

The role of cyclic adenosine monophosphate, or cAMP, is pivotal in the process of smooth muscle relaxation, especially concerning the bronchi. When epinephrine binds to beta-2 adrenergic receptors, it ultimately leads to an increase in cAMP levels within the smooth muscle cells. Increased cAMP production is a result of the activation of an enzyme called adenylyl cyclase, which is stimulated by the receptor.

• cAMP serves as a secondary messenger that transmits the signal from epinephrine to the inside of the cell.
• This high level of cAMP initiates processes that lower intracellular calcium concentrations.

Lower calcium levels lead to muscle relaxation because calcium ions are necessary for muscle contraction. By reducing the availability of calcium, cAMP helps to promote relaxation of the airway smooth muscles, facilitating easier breathing. This mechanism is central to understanding how medications leveraging the cAMP pathway can effectively serve as bronchodilators, providing relief in instances of respiratory distress.