Comprehensive Study Notes on Blood Pressure Control and Its Physiology
What is Blood Pressure?
Blood pressure (BP) is defined as the ratio between the pressure in the arteries during two specific physiological states:
Systolic pressure: The pressure in the arteries when the heart is actively pumping (during contraction).
Diastolic pressure: The pressure in the arteries when the heart is at rest (during filling).
BP serves as a measure of how effectively the heart is functioning and reflects the pressure in the arteries overall.
Blood Vessels: Need for Balance
Maintaining blood pressure involves a balance between vessel constriction and dilation.
Vasoconstriction: The narrowing of blood vessels, leading to increased blood pressure.
Vasodilation: The widening of blood vessels, resulting in decreased blood pressure.
Anatomy of a Blood Vessel
Blood vessel structure: Includes two primary types:
Arteries: Carry oxygen-rich blood away from the heart.
Veins: Carry oxygen-poor blood back to the heart.
Understanding Receptors and Channels
What are Receptors?
Receptors are proteins found on cell surfaces that, when activated, trigger cellular responses. Antagonist( stops something from happening) vs. Agonist (causes something to happen).
Effects of Blocking a Receptor:
Blocking a receptor prevents the usual response from occurring, acting as an antagonist.
What is a Channel? - Proteins pass through a channel
Channels are proteins that facilitate the passage of substances in and out of cells. They allow specific molecules, such as ions or water, to cross the cellular membrane.
Effects of Blocking/ Causing A reaction in a channel:
Blocking a channel prevents the flow of the substance between cellular compartments, acting as an antagonist.
Causing a reaction in a channel is agonist.
Examples of Receptors and Channels
Receptor Types:
Beta 1 receptors (1 heart = Beta 1): Located in the heart, activated by epinephrine and norepinephrine, increase heart rate.
Beta 2 receptors ( 2 lungs= Beta 2) : Found in the lungs, also activated by epinephrine and norepinephrine, facilitate bronchodilation and vasodilation.
Alpha receptors: Associated with peripheral arteries (arms, legs), activated by norepinephrine and epinephrine, cause vasoconstriction.
Angiotensin II receptors: Activated by angiotensin II, play a significant role in blood pressure regulation.
Vasopressin receptors: Respond to vasopressin, impacting blood pressure through various mechanisms.
Channels:
Calcium channels: Facilitate the entry of calcium ions into cells which is crucial for various cellular functions (e.g., muscle contractions).
Pathophysiology of Blood Pressure Control
1. Renin-Angiotensin/Aldosterone System (RAAS)
A critical hormone system for blood pressure regulation.
Function: Helps maintain blood pressure and fluid balance.
2. Vasopressin System of BP Control
Regulates blood pressure through water retention and vasodilation or vasoconstriction.
3. Sympathetic Nervous System Activation
Low blood volume or blood pressure is detected by baroreceptors located in the aorta and carotid arteries.
Baroreceptors send signals to the brain, which then prompt the brain to signal adrenal medulla to produce:
Epinephrine (more stronger, greater effect in Beta 1) : Increases heart rate.
Norepinephrine: Causes vasoconstriction, increasing blood pressure.
Where is epinephrine and Norepinephrine made? Adrenal medulla
Both Epinephrine and Norepinephrine causes constriction
Adrenal Glands and Their Functions
Anatomy Overview:
Comprised of three sections: capsule, medulla, and cortex.
Actions of the Sympathetic Nervous System
Upon stimulation:
Beta-1 receptors increase heart rate.
Beta-2 receptors cause bronchodilation and vasodilation. Help you breathe easier. Gas exchange better due to adequate blood flow.
Alpha receptors are stimulated (agonist) to facilitate vasoconstriction and increase venous return.
Renin-Angiotensin-Aldosterone System (RAAS) Explained
Pathway:
Low blood volume blood vessels dilate due to blood loss or infection, sensed by kidneys leads to renin production.
Renin converts angiotensinogen to angiotensin I.
Angiotensin I is converted into angiotensin II by angiotensin-converting enzyme (ACE). You need ACE to convert angiotensin I to angiotensin II.
Activation of Angiotensin II:
Angiotensin II activates specific receptors on blood vessels, resulting in:
Vasoconstriction.
Increased blood pressure.
Increased venous return (increased blood flow) to the heart.
Aldosterone's Role in BP Control
Secretion: Aldosterone is released from the adrenal cortex in response to high levels of angiotensin II and norepinephrine.
Function: Tells kidney tubules to retain water and sodium, resulting in increased blood volume and, consequently, increased blood pressure.
Neurohormonal Activation and Vasopressin
Vasopressin (ADH):
Synthesized in the hypothalamus and stored in posterior pituitary gland.
Released in response to low circulatory volume and elevated levels of epinephrine, norepinephrine, and angiotensin II.
Function of Vasopressin:
Activates V1, V2, V3 receptors, leading to vasoconstriction and increased blood pressure.
Activates V2 receptors in the kidneys to increase water reabsorption, further raising blood pressure.
If the BP is high, then Vasopressin continue to operate, causing BP to continue to rise. An antagonist(blocker) is needed to stop BP rise.
Calcium Channels in the Cardiovascular System
Heart:
Calcium channels, when activated, cause the heart to beat faster and increase the strength of contractions.
Effects of Blocking Calcium Channels:
Slows heart rate and decreases contraction strength.
Blood Vessels:
Calcium channels, when stimulated, lead to contraction of vascular smooth muscle, raising blood pressure.
Effects of Blocking Calcium Channels:
Causes dilation of blood vessels, reducing blood pressure.
Reasoning and Clinical Implications
Key Questions to Consider:
What happens when beta 1 receptors are activated or blocked?
What happens when beta 2 receptors are activated or blocked?
What happens when alpha receptors are activated or blocked?
What happens when calcium channels are activated or blocked?
Pathophisiology and how to treat hypertension with this info?