Overview
This lecture covers how the autonomic nervous system regulates heart rate and contractility through sympathetic and parasympathetic pathways, focusing on key electrophysiological mechanisms.
Autonomic Innervation of the Heart
- The heart receives input from both the parasympathetic (vagus nerve) and sympathetic nervous systems.
- The vagus nerve innervates the SA node, AV node, and atria, but minimally affects the ventricles.
- The sympathetic nervous system innervates the entire heart, including the ventricles.
Key Autonomic Effects on the Heart
- Chronotropic effects refer to changes in heart rate.
- Dromotropic effects refer to changes in conduction velocity through the heart.
- Inotropic effects refer to changes in cardiac contractility.
- Lusitropy refers to the heart's ability to relax.
Sympathetic vs. Parasympathetic Effects: Mechanisms
- Sympathetic activation increases heart rate (chronotropy), conduction velocity (dromotropy), and contractility (inotropy) mainly via beta-1 receptors, increasing funny current (If) and calcium current (ICa).
- Parasympathetic activation (acetylcholine) decreases heart rate, conduction, and contractility by reducing funny current and calcium current, and increasing potassium current (IK).
Mechanisms of Heart Rate Modulation
- Parasympathetic stimulation slows depolarization of the SA node and conduction in the AV node.
- Heart rate can be slowed by:
- Decreasing the slope of Phase 4 depolarization.
- Hyperpolarizing the maximum diastolic (resting membrane) potential.
- Raising the threshold for action potential initiation.
- Increased potassium current (IK) is primarily responsible for hyperpolarization.
Dromotropy and Conduction Velocity
- Dromotropic changes are mainly observed in the AV node.
- Sympathetic stimulation increases AV node conduction by shortening the effective refractory period via increased calcium current.
- Strong parasympathetic stimulation can slow AV node conduction to the point of causing heart block.
Inotropic Effects and Contractility
- Cardiac contractility is controlled by intracellular calcium levels, not by recruitment as in skeletal muscle.
- Contractility depends on calcium influx from the extracellular space and release from the sarcoplasmic reticulum (SR).
- Calcium channel blockers decrease contractility by reducing inward calcium current.
- Sympathetic stimulation via β-receptors activates cAMP and PKA, leading to increased calcium influx and release from the SR.
- PKA also enhances SERCA activity via phospholamban phosphorylation, speeding relaxation (lusitropy) and increasing SR calcium storage for future contractions.
Key Terms & Definitions
- Chronotropy — heart rate modulation.
- Dromotropy — conduction velocity modulation.
- Inotropy — contractility modulation.
- Lusitropy — relaxation ability of the heart.
- Funny current (If) — ion current responsible for pacemaker activity in the SA node.
- SA node — primary heart pacemaker.
- AV node — relays impulses from atria to ventricles.
- Sarcoplasmic reticulum (SR) — intracellular calcium store.
Action Items / Next Steps
- Review the comparison table of sympathetic vs. parasympathetic effects on cardiac function.
- Study the molecular mechanisms of PKA in cardiac myocytes.
- Prepare for exam questions on the three mechanisms of heart rate modulation.