15.2 Autonomic Reflexes and Homeostasis

Autonomic Nervous System Reflexes

Somatic vs. Autonomic Reflex Arcs

Both somatic and autonomic reflexes follow the basic reflex arc pattern (receptor → afferent neuron → integration center → efferent neuron → effector), but they differ in their pathways and targets.

Somatic reflex arcs are relatively simple. The afferent neuron synapses directly with (or through a single interneuron to) the efferent somatic motor neuron in the spinal cord or brainstem. That motor neuron then travels directly to a skeletal muscle effector. There's one neuron on the efferent side, and it's always excitatory.

Autonomic reflex arcs are more complex in two key ways:

• The effectors are smooth muscle, cardiac muscle, or glands rather than skeletal muscle.
• The efferent pathway always involves two neurons in series: a preganglionic neuron (cell body in the CNS) synapses with a postganglionic neuron (cell body in an autonomic ganglion outside the CNS), which then reaches the effector tissue. Interneurons in the CNS are also typically part of the integration step.

This two-neuron chain on the efferent side is the structural hallmark that distinguishes autonomic from somatic reflex arcs.

Sympathetic vs. Parasympathetic Reflexes

These two divisions generally oppose each other to fine-tune organ function. Most visceral organs receive dual innervation from both divisions.

Sympathetic ("fight or flight") reflexes:

• Increase heart rate and contractility
• Dilate bronchioles (easier breathing)
• Decrease digestive activity
• Constrict blood vessels in the skin and digestive organs
• Dilate blood vessels in skeletal muscles
• Stimulate glucose release from the liver

Parasympathetic ("rest and digest") reflexes:

• Decrease heart rate and contractility
• Constrict bronchioles
• Increase digestive activity (motility and secretion)
• Stimulate salivation and other glandular secretions
• Promote glucose storage in the liver

Autonomic Reflex Pathways and Regulation

Short vs. Long Autonomic Reflexes

Short reflexes operate through local circuits within a single organ, without involving the CNS. The enteric nervous system of the GI tract is the best example. When the intestinal wall stretches, local enteric neurons detect this and stimulate peristalsis on their own. The signal never has to travel to the spinal cord or brain.

Long reflexes route through the CNS and can coordinate responses across multiple organs. The baroreceptor reflex is a classic example:

1. Baroreceptors in the aortic arch and carotid sinuses detect a change in blood pressure (say, a drop).
2. Afferent neurons carry this signal to the cardiovascular center in the medulla oblongata.
3. The medulla adjusts autonomic output: it increases sympathetic signaling and decreases parasympathetic signaling.
4. Efferent signals raise heart rate, increase contractility, and constrict blood vessels, bringing blood pressure back toward normal.

This is a long reflex because it involves a sensory receptor far from the CNS, central processing, and efferent signals back out to multiple effectors.

Autonomic Neurotransmitters and Receptors

Understanding which neurotransmitter binds which receptor is essential for predicting autonomic effects.

Acetylcholine (ACh):

• Released by all preganglionic neurons (both sympathetic and parasympathetic)
• Released by postganglionic parasympathetic neurons
• Binds nicotinic receptors on postganglionic neuron cell bodies (in ganglia)
• Binds muscarinic receptors on effector tissues (heart, smooth muscle, glands)

Norepinephrine (NE):

• Released by most postganglionic sympathetic neurons
• Binds $\alpha$-adrenergic receptors, which typically cause vasoconstriction and smooth muscle contraction
• Binds $\beta$-adrenergic receptors, which typically cause bronchodilation ($\beta_2$), increased heart rate and contractility ($\beta_1$), and vasodilation in some tissues

Notable exceptions:

• Some sympathetic postganglionic neurons release ACh instead of NE (e.g., those innervating sweat glands and blood vessels in skeletal muscles)
• The adrenal medulla acts like a modified sympathetic ganglion: preganglionic sympathetic neurons synapse directly on chromaffin cells, which release epinephrine and NE into the bloodstream as hormones, amplifying and prolonging sympathetic effects throughout the body

Drug Impacts on Autonomic Function

Drugs that target autonomic receptors or neurotransmitter metabolism are widely used in medicine. They fall into a few major categories:

Cholinergic drugs (enhance parasympathetic-like effects):

1. Muscarinic agonists (e.g., pilocarpine) mimic ACh at muscarinic receptors. Effects can include bradycardia, bronchoconstriction, and increased digestive activity. Pilocarpine is commonly used to treat glaucoma by constricting the pupil.
2. Anticholinesterases (e.g., physostigmine) inhibit acetylcholinesterase, the enzyme that breaks down ACh. This prolongs ACh activity at the synapse. These drugs are used to treat myasthenia gravis, a condition of skeletal muscle weakness caused by impaired neuromuscular transmission.

Adrenergic drugs (enhance sympathetic-like effects):

1. Sympathomimetics (e.g., ephedrine) mimic NE/epinephrine at adrenergic receptors, producing tachycardia, bronchodilation, and vasoconstriction. Albuterol is a $\beta_2$-selective sympathomimetic used for asthma.
2. $\beta$-blockers (e.g., propranolol) block $\beta$-adrenergic receptors, reducing sympathetic stimulation of the heart and lungs. They're prescribed for hypertension, angina, and arrhythmias.

Autonomic blockers (reduce parasympathetic or sympathetic effects):

1. Muscarinic antagonists (e.g., atropine) block ACh at muscarinic receptors, reducing parasympathetic tone. This can cause tachycardia, bronchodilation, decreased secretions, and pupil dilation. Atropine is used during certain cardiac emergencies and eye exams.
2. $\alpha$-blockers (e.g., phentolamine) block $\alpha$-adrenergic receptors on blood vessels, reducing sympathetic vasoconstriction. They're used to treat hypertension and peripheral vascular disease.

Homeostatic Mechanisms and Feedback Systems

Negative Feedback

Most autonomic reflexes operate through negative feedback, where the response counteracts the original stimulus to restore a set point. The baroreceptor reflex described above is a perfect example: a drop in blood pressure triggers responses that raise it back up, and once pressure is restored, the stimulus diminishes and the response tapers off.

Another example: when body temperature rises above its set point (~37°C), the hypothalamus triggers vasodilation in the skin and sweating. These responses cool the body, bringing temperature back down. Once the set point is reached, the cooling responses decrease.

Positive Feedback

Positive feedback amplifies the original stimulus rather than counteracting it. These loops are far less common and typically drive a process to completion rather than maintaining a stable state.

The classic example is childbirth: pressure of the baby's head on the cervix stimulates oxytocin release, which strengthens uterine contractions, which increases pressure on the cervix, which triggers more oxytocin. The cycle only ends when the baby is delivered and the stimulus is removed.