Hormonal and Neural control of Blood pressure Flashcards
What is blood pressure and how is it calculated?
Blood pressure (BP) is the force exerted by blood on arterial walls.
Equation: BP = CO × TPR
CO (Cardiac Output) = HR × SV
TPR (Total Peripheral Resistance) = Resistance in systemic circulation
What factors determine total peripheral resistance (TPR)?
- Arteriolar smooth muscle tone (Vasoconstriction increases TPR, vasodilation decreases it).
- Blood viscosity (Thicker blood = more resistance).
- Blood vessel length (Longer vessels = more resistance).
- Arterial cross-sectional area (Smaller arteries = higher resistance).
Where are baroreceptors located, and what do they detect?
Location:
- Carotid sinus (internal carotid artery, above bifurcation).
- Aortic arch (detects systemic BP changes).
Function:
- Detect arterial stretch, which reflects blood pressure changes.
- Increased stretch = High BP → Increased baroreceptor firing.
- Decreased stretch = Low BP → Reduced baroreceptor firing.
What is the neural pathway of the baroreceptor reflex?
- Baroreceptors (Carotid sinus & Aortic arch) → Nucleus of the Solitary Tract (NTS) in Medulla (receives input).
- NTS → Rostral Ventrolateral Medulla (RVLM) → Sympathetic Activation (if BP is low).
- NTS → Nucleus Ambiguus → Parasympathetic (Vagal) Activation (if BP is high).
- Effect: Modulates vascular tone & heart rate to stabilize BP.
What happens in the baroreceptor reflex when blood pressure falls (hypotension)?
- Less stretch on baroreceptors → Reduced firing rate.
- NTS signals to the RVLM → Increased sympathetic activity.
- Effects:
- Arteriolar constriction → ↑ TPR → ↑ BP.
- Increased heart rate & contractility → ↑ CO → ↑ BP.
What happens in the baroreceptor reflex when blood pressure increases (hypertension)?
- Increased stretch on baroreceptors → Increased firing rate.
- Inhibits RVLM → Reduced sympathetic activity.
- Effects:
- Vasodilation → ↓ TPR → ↓ BP.
- Heart rate decreases (via vagal activation) → ↓ CO → ↓ BP.
What are the steps of the RAAS pathway?
- Renin (Kidneys) converts angiotensinogen (Liver) → Angiotensin I.
- Angiotensin-Converting Enzyme (ACE) (Lungs) converts Angiotensin I → Angiotensin II.
- Angiotensin II effects:
- Vasoconstriction → Increases BP.
- Aldosterone release → Sodium & water retention → Increases BP.
- ADH release → Water retention → Increases BP.
- Stimulates thirst → Increases BP.
What is the function of aldosterone, and where is it released from?
Function: Increases sodium & water reabsorption in the distal tubule & collecting duct.
Released from: Adrenal cortex.
How does antidiuretic hormone (ADH, Vasopressin) regulate blood pressure?
- Increases water reabsorption in the kidneys.
- Promotes vasoconstriction to raise BP.
- Released from the posterior pituitary gland.
A 68-year-old woman has severe blood loss. Her BP is 85/50 mmHg, and HR is 120 bpm. What short-term BP regulation system is activated?
Baroreceptor Reflex: Increases HR & vasoconstriction to restore BP.
A 75-year-old man experiences dizziness when standing. His BP drops from 120/80 to 90/60 mmHg, and HR increases from 70 to 110 bpm. What condition is he experiencing?
Orthostatic Hypotension – BP drops due to delayed baroreceptor reflex activation.
A patient with chronic hypertension is prescribed an ACE inhibitor. How does this medication lower BP?
Blocks Angiotensin-Converting Enzyme (ACE) → Prevents Angiotensin II formation.
No vasoconstriction → BP decreases.
How does chronic heart failure affect BP regulation?
- RAAS is overactivated, leading to fluid retention & increased afterload.
- Baroreceptor reflex is blunted, causing inappropriate BP regulation.
A patient with chronic hypertension is prescribed an ACE inhibitor. How does this medication lower BP?
Blocks Angiotensin-Converting Enzyme (ACE) → Prevents Angiotensin II formation.
No vasoconstriction → BP decreases.
How does chronic heart failure affect BP regulation?
RAAS is overactivated, leading to fluid retention & increased afterload.
Baroreceptor reflex is blunted, causing inappropriate BP regulation.