Cardiovascular Effects of the Autonomic Nervous System (ANS)

Cardiovascular Effects of the Autonomic Nervous System (ANS)

Learning Objectives

  1. Explain how the ANS regulates CV function.
  2. Describe mechanisms of short-term blood pressure control and explain the role of baroreceptors.
  3. Explain how prototype sympathomimetics affect blood pressure and heart rate.

Autonomic Nervous System (ANS)

The ANS regulates cardiovascular (CV) function through its two main divisions: the sympathetic and parasympathetic nervous systems, each impacting various organs like the eyes, heart, lungs, and more in different ways.

Parasympathetic vs. Sympathetic Comparison

  • Parasympathetic System: Constricts pupils, stimulates salivation, slows the heartbeat, constricts bronchi, stimulates digestion, stimulates bile release, and contracts the bladder.
  • Sympathetic System: Dilates pupils, inhibits salivation, accelerates heartbeat, dilates bronchi, inhibits digestion, stimulates glucose release, stimulates epinephrine, and norepinephrine release, and relaxes the bladder.

The Sympathetic Nervous System

  • Heart: Accelerates heartbeat, increases conduction velocity, and enhances contractility.
  • Blood Vessels: Causes generalized vasoconstriction, with exceptions like vasodilation in skeletal muscles.
  • Lungs: Dilates bronchi.
  • Metabolism: Increases gluconeogenesis, glycogenolysis, and lipolysis.
  • Glands and Organs: Promotes sweat secretion and inhibits digestive activity.

The Parasympathetic Nervous System

  • Heart: Slows heartbeat and reduces conduction velocity.
  • Blood Vessels: Promotes vasodilation in specialized tissues.
  • Lungs: Constricts bronchi.
  • Digestive System: Stimulates activity in the gastrointestinal tract.
  • Glands: Promotes secretion in salivary and nasopharyngeal glands.

Mechanisms of Blood Pressure Regulation

1. Sympathetic Innervation

  • Blood Vessels: Arteries and veins are innervated only by the sympathetic system. Increased activity causes vasoconstriction (α1 receptors) in major vascular beds and vasodilation in skeletal muscle arterioles (β2 receptors).
  • Heart: Sympathetic nerves enhance heart rate and contractility via β1 receptors. Parasympathetic effects via vagus nerve (M2 receptors) decrease heart rate.

2. Adrenergic Receptor Subtypes and Intracellular Mechanisms

  • α1 Receptors: Linked with Gq proteins, increase IP3 and DAG, leading to increased intracellular Ca2+ and vasoconstriction.
  • α2 Receptors: Associated with Gi proteins, decrease cAMP, and reduce norepinephrine release.
  • β1 Receptors: Stimulatory effects, increase cAMP, enhancing heart rate, contractility, and renin release.
  • β2 Receptors: Also increase cAMP, but primarily causing vasodilation and bronchodilation.
[himg]impact of sympathetic nervous system[/himg]

3. Baroreceptors

  • Located in the carotid sinus and aortic arch, baroreceptors detect changes in arterial pressure. Increased pressure stretches baroreceptors, increasing their firing rate. This activates a negative feedback loop involving the vagus nerve and medulla, reducing sympathetic outflow and increasing parasympathetic activity to decrease blood pressure and heart rate.
  • Conversely, decreased pressure lowers baroreceptor firing, increasing sympathetic activity and decreasing parasympathetic output, raising blood pressure and heart rate to normal levels.

Frank-Starling Law

This law states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (end-diastolic volume or EDV). Mechanisms include:

  • Increased EDV stretches the ventricular walls, leading to a more forceful contraction.
  • Greater stroke volume ultimately generates higher cardiac output.
  • Factors influencing this include preload, afterload, and contractility.

Clinical Applications

Sympathomimetics in Cardiac Care:

  • Dobutamine/Dopamine: Used in acute heart failure or shock to increase cardiac contractility and reduce afterload through minor β2 effects, though they may cause arrhythmias.
  • Norepinephrine (NE): Increases blood pressure primarily through α1-mediated vasoconstriction, also affecting β1 receptors in the heart.
  • Phenylephrine: Utilized as a nasal decongestant due to its α1 agonist properties.
  • Clonidine: An α2 agonist used to decrease blood pressure through CNS effects.

Adrenergic Drug Effects:

  • Epinephrine: Acts on α1, α2, β1, and β2 receptors, causing increased heart rate, contractility, vasoconstriction, and vasodilation.
  • Norepinephrine: Influences α1, α2, and β1 receptors, enhancing heart contractility and causing vasoconstriction without β2 actions.
  • Isoproterenol: Stimulates β1 and β2 receptors, leading to increased heart rate and contractility with vasodilation.

Hormonal Regulation - RAAS

The Renin-Angiotensin-Aldosterone System (RAAS) significantly influences blood pressure and fluid balance:

  • Renin: Released from kidneys in response to low blood pressure or sympathetic activation.
  • Angiotensin II: Formed through Angiotensin I conversion by ACE; it elevates blood pressure via vasoconstriction and stimulates aldosterone release.
  • Aldosterone: Promotes sodium and water retention, increasing blood volume and preload, thus raising blood pressure.

Key highlights involve the role of AT1 receptors and ACE inhibition in therapeutics.