Nervous and Local Control of the Bronchioles:

Nervous and Local Control of the Bronchioles:
1. Sympathetic dilation of the bronchioles: Direct control of the bronchioles by sympathetic nerve fibers is relatively weak because few of these fibers penetrate to the central portions of the lung. However, the bronchial tree is very much exposed to norepinephrine and epinephrine released into the blood by sympathetic stimulation of the adrenal gland medullae. Both these hormones— especially epinephrine, because of its greater stimulation of beta-adrenergic receptors—cause dilation of the bronchial tree.

2.Parasympathetic constriction of the bronchioles:
A few parasympathetic nerve fibers derived from the vagus nerves penetrate the lung parenchyma. These nerves secrete acetylcholine and, when activated, cause mild to moderate constriction of the bronchioles. When a disease process such as asthma has already caused some bronchiolar constriction, superimposed parasympathetic nervous stimulation often worsens the condition. When this occurs, administration of drugs that block the effects of acetylcholine, such as atropine, can sometimes relax the respiratory passages enough to relieve the obstruction.
Several substances formed in the lungs themselves are often quite active in causing bronchiolar constriction.
Two of the most important of these are histamine and slow reactive substance of anaphylaxis. Both of these are released in the lung tissues by mast cells during allergic reactions, especially those caused by pollen in the air. Therefore, they play key roles in causing the airway obstruction that occurs in allergic asthma; this is especially true of the slow reactive substance of anaphylaxis.
The same irritants that cause parasympathetic constrictor reflexes of the airways—smoke, dust, sulfur dioxide, and some of the acidic elements in smog—often act directly on the lung tissues to initiate local, non-nervous
reactions that cause obstructive constriction of the airways.