"

Chapter 7 Selected Diseases and Disorders of the Cardiovascular System

7.1i Neural and Hormonal Regulation of Blood Pressure

Zoë Soon

The body uses both Neural and Hormonal Mechanisms to control Systemic Blood Pressure and Cardiac Output.

Both neural and hormonal regulation mechanisms are required in order to maintain adequate perfusion throughout the body, in a manner that is responsive to various daily activities (e.g., standing up, sitting down, running, thinking hard etc.)

Blood Pressure Homeostasis Regulatory Mechanisms:

  • Chemoreceptors and Baroreceptors in the carotid sinus and aortic arch monitor blood oxygen and pressure.  Chemoreceptors are also located on the ventrolateral surface of the medulla oblongata.
  • Chemoreceptors: monitor blood levels of O2, CO2 and pH.
  • Baroreceptors: monitor blood pressure in the carotid sinus and aortic arch.
  • The medulla oblongata uses that information to adjust heart rate, heart contractility (force of contraction), and vascular tone to stabilize blood pressure.
    • Adjustments made by the brain (cardiovascular centers in the medulla oblongata):
      • Heart Rate: Speeds up or slows down (via sympathetic or parasympathetic pathways respectively)
      • Force of Contraction: Increases or decreases (via sympathetic or parasympathetic pathways respectively), which modulates stroke volume.
      • Vascular Tone: Vasocontrict (via sympathetic pathway) or vasodilate to adjust resistance and blood flow.
  • The body constantly makes adjustments to heart rate, stroke volume, and vascular tone (vasodilation/vasoconstriction), to ensure tissues receive sufficient blood, oxygen, and nutrients and can also facilitate the removal of waste products produced by cells.

Sympathetic Response (“Fight or Flight”)

  • Via Cardiac Accelerator Nerve releasing neurotransmitters:
    • Epinephrine (E) and norepinephrine (NE) are released and bind to:
    • Beta-1 adrenergic receptors on the Sinoatrial (SA) node, which opens more Ca++ channels, bringing cardiomyocytes closer to threshold:
      • Increase depolarization rate, speeding heart rate (“beat” the heart faster).
      • Increase force of contraction (positive inotropy).
    • Alpha-1 adrenergic receptors in arteries:
      • Cause vasoconstriction, increasing resistance and BP.
  • Memory trick:
    • A’s for alpha-1 adrenergic receptors in arterial walls (vasoconstriction).
    • B’s for beta in the beating heart (speeding heart rate).

Parasympathetic Response (“Rest and Digest”)

  • Via vagus nerve (cranial nerve X):
    • Releases acetylcholine (ACh) which bind to muscarinic receptors in the SA node.
    • Stimulating the opening of potassium channels, hyperpolarizing cells, which slows depolarization and decreases HR.
    • Reduces force of contraction (heart contractility) and overall cardiac output.

Heart Medications that Modulate Heart Rate and Contractility

Beta-adrenergic Receptors and Beta-Blocker Drugs:

  • Beta-1 adrenergic receptors: Located in the SA node of the heart.
  • Beta-blockers: Drugs that block these receptors, preventing sympathetic stimulation.
  • Function of beta-1 blockade:
    • Prevents epinephrine/norepinephrine from increasing heart rate and contractility.
    • Result: Slower heart rate and reduced force of contraction, giving the heart a “rest” to recover, especially beneficial in damaged hearts.  However, can mean that person becomes more exercise-intolerant (unable to elevate heart rate and contractility required for moderate-vigourous physical activity), a condition that can be desirable if a person’s heart is damaged or has reduced perfusion due to blocked/narrowed coronary arteries.
  • In contrast, beta-2 adrenergic receptors are in other tissues (like bronchioles), but they are not targeted in cardiovascular therapies.  This is beneficial as sympathetic-induced bronchodilation via epinephrine/norepinephrine is still possible.

 

Blood Volume Regulation and Hormones

  • Blood volume influences BP proportionality:
    • Increased volume elevates BP; decreased volume lowers BP.
  • Kidneys:
    • Responsible for regulating blood volume via urine output.
  • Antidiuretic hormone (ADH):
    • Increases blood volume by promoting water reabsorption in kidneys.
    • Causes vasoconstriction, raising BP.
  • Aldosterone:
    • Promotes salt and water retention, increasing blood volume and BP.
    • Decreases urine output.
  • Renin-Angiotensin System:
    • When BP drops, kidneys release renin.
    • Renin converts angiotensinogen into

License

Share This Book