Autonomic Control of the Heart

Overview of Cardiac Autonomic Regulation

The heart possesses intrinsic mechanisms for generating rhythmic contractions, but the autonomic nervous system (ANS) modulates cardiac activity to meet physiological demands. The effects of autonomic input depend on the neurotransmitter released, the receptor activated, and the specific cardiac tissue targeted.

• Intrinsic Cardiac Activity: The heart can generate its own rhythm (automaticity) without requiring direct nervous input for each beat.

• Autonomic Modulation: The ANS adjusts heart rate, contractile force, and conduction velocity to adapt to changing bodily needs.

Divisions of the Autonomic Nervous System

The ANS consists of two main divisions with generally opposing effects on the heart:

• Sympathetic Division: Prepares the body for increased activity ("fight or flight").

• Parasympathetic Division: Promotes rest and conservation of energy ("rest and digest").

Autonomic Neural Pathways to the Heart

The neural pathway for autonomic control of the heart differs from the somatic motor pathway:

• Somatic Motor Pathway: CNS → motor neuron (ventral horn) → skeletal muscle

• Autonomic Motor Pathway: CNS → preganglionic neuron → autonomic ganglion → postganglionic neuron → cardiac tissue

• CNS: Integrates information and regulates autonomic output.

• Preganglionic Neuron: Cell body in CNS; axon projects to autonomic ganglion.

• Autonomic Ganglion: Relay station containing postganglionic neuron cell bodies.

• Postganglionic Neuron: Axon projects from ganglion to target tissue (e.g., heart).

• Cardiac Targets: Pacemaker tissue (SA node), conduction tissue (AV node), contractile myocardium.

Neurotransmitters and Receptors in Cardiac Autonomic Control

The effects of autonomic stimulation depend on the neurotransmitter released and the receptor type present on cardiac tissue.

• Preganglionic Neurons (Both Divisions): Release acetylcholine (ACh) at the autonomic ganglion, which binds to nicotinic acetylcholine receptors on postganglionic neurons.

• Sympathetic Postganglionic Neurons: Release norepinephrine (NE) at cardiac targets, primarily activating β1-adrenergic receptors.

• Parasympathetic Postganglionic Neurons: Release ACh at cardiac targets, primarily activating muscarinic M2 receptors.

Summary Table: Neurotransmitters and Receptors in Cardiac Autonomic Pathways

Functional Effects of Autonomic Input on the Heart

• Sympathetic Effects:

  • Increases heart rate (positive chronotropy)

  • Increases ventricular contractile force (positive inotropy)

  • Increases AV nodal conduction (positive dromotropy)

• Parasympathetic Effects:

  • Decreases heart rate (negative chronotropy), especially via the SA node

  • Decreases AV nodal conduction (negative dromotropy)

  • Minimal direct effect on ventricular contractile force

Key Terms: Chronotropy, Inotropy, Dromotropy

• Chronotropy (Rate): Refers to the rate of cardiac activity, especially heart rate.

  • Positive chronotropic effect: Increases heart rate

  • Negative chronotropic effect: Decreases heart rate

  • SA node is the primary site for chronotropic effects

• Inotropy (Force): Refers to the force of cardiac contraction.

  • Positive inotropic effect: Increases contractile force

  • Negative inotropic effect: Decreases contractile force

  • Sympathetic stimulation has a strong positive inotropic effect on ventricular myocardium

• Dromotropy (Conduction): Refers to the speed of electrical conduction through cardiac tissue, especially the AV node.

  • Positive dromotropic effect: Increases conduction velocity

  • Negative dromotropic effect: Decreases conduction velocity

  • AV node is the primary site for dromotropic effects

Examples and Applications

• Increased Sympathetic Activity: During exercise, sympathetic stimulation increases heart rate, contractile force, and conduction velocity to support increased cardiac output.

• Increased Parasympathetic (Vagal) Activity: At rest, parasympathetic input via the vagus nerve slows heart rate and AV nodal conduction, conserving energy.

• Clinical Application: Drugs that block β1-adrenergic receptors (beta-blockers) are used to decrease heart rate and contractility in conditions like hypertension.

Common Misconceptions Clarified

• Intrinsic Pacemaker Activity: The heart does not require a new command from the brain for each beat; the SA node generates rhythmic impulses.

• Neurotransmitter Effects: Both divisions use ACh at ganglia, but their effects differ at the cardiac target due to different receptors (nicotinic vs. muscarinic).

• Sympathetic Effects: Sympathetic activity affects not only heart rate but also contractility and conduction.

• Parasympathetic Effects: Parasympathetic activity slows but does not stop the heart.

• Distinct Terms: Chronotropy, inotropy, and dromotropy refer to different physiological variables (rate, force, conduction).

• AV Node vs. SA Node: Slower AV conduction does not necessarily mean a slower SA node (pacemaker) rate.

• Receptor and Tissue Specificity: The effect of a neurotransmitter depends on the receptor type and the target tissue.

Practice Questions

1. Which neurotransmitter is released by both sympathetic and parasympathetic preganglionic neurons?

2. Which receptor is activated by NE in the typical sympathetic pathway to the heart?

3. Which receptor is activated by ACh released from parasympathetic postganglionic neurons at cardiac targets?

4. Define chronotropy, inotropy, and dromotropy.

5. A drug increases activation of cardiac β1 receptors. Predict the typical effects on heart rate, ventricular contractility, and AV nodal conduction.

6. Increased vagal activity slows heart rate. Identify the postganglionic neurotransmitter and receptor responsible for the typical cardiac response.

7. A student claims that parasympathetic activity should increase heart rate because ACh is released by both autonomic divisions at their ganglia. Identify the reasoning error.

8. An experimental intervention slows AV nodal conduction without directly changing SA nodal pacing. Which functional effect has changed, and which has not necessarily changed?

9. A hypothetical drug blocks M2 receptors in the heart. Predict how this would affect the ability of parasympathetic activity to slow heart rate. Explain your reasoning without describing an intracellular signaling cascade.

10. A patient has increased sympathetic activity. Explain why “the heart beats faster” is an incomplete description of the possible cardiac response.

Application Scenario: Increased Vagal Activity

Question: Explain how increased vagal activity produces decreased heart rate and slowed AV nodal conduction. Consider the neural pathway, neurotransmitter, receptor, and functional effects.

• Neural Pathway: Parasympathetic (vagal) preganglionic neuron (CNS) → autonomic ganglion → postganglionic neuron → heart

• Neurotransmitter at Cardiac Target: Acetylcholine (ACh)

• Receptor Activated: Muscarinic M2 receptor

• Functional Effects: Decreased heart rate (negative chronotropy) and slowed AV nodal conduction (negative dromotropy)

Additional info: The vagus nerve provides approximately 75% of parasympathetic input to the heart, and "vagal activity" is often used interchangeably with "parasympathetic activity."