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Short-Term and Long-Term Regulation of Blood Pressure

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INTRODUCTION

• Short-term regulation - acts within seconds to minutes (mainly via nervous system)
• Long-term regulation - acts over hours to days (mainly via kidneys and hormones)

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PART 1: SHORT-TERM REGULATION OF BLOOD PRESSURE

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1. Baroreceptor Reflex (Most Important Short-Term Mechanism)

• Stretch-sensitive nerve endings in the walls of carotid sinus (just above carotid bifurcation) and aortic arch
• They fire nerve impulses when BP rises (vessel wall is stretched)

BP rises → baroreceptors stretch → more impulses sent to medulla → inhibit vasomotor center + activate vagus → vasodilation + decreased HR and contractility → BP falls back to normal

BP falls → baroreceptors less stretched → fewer impulses → vasomotor center activated → vasoconstriction + increased HR → BP rises back to normal

• Carotid sinus signals → Hering's nerve → Glossopharyngeal nerve → Nucleus Tractus Solitarius (NTS) in medulla
• Aortic arch signals → Vagus nerve → NTS
• NTS → inhibits vasomotor (vasoconstrictor) center and excites vagal cardioinhibitory center

• Baroreceptors respond in a fraction of a second - fastest BP control
• They respond more to rapidly changing pressure than steady pressure
• Most sensitive in the 60-180 mm Hg range
• This is a negative feedback system
• Baroreceptors adapt within 1-2 days, so they cannot maintain long-term BP control

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2. Chemoreceptor Reflex

• This is mainly a backup to baroreceptors
• Especially important when BP drops below 60-80 mm Hg (range where baroreceptors become less effective)

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3. CNS Ischemic Response (Last Resort / Emergency)

• When blood flow to the brain itself drops critically (BP < 60 mm Hg)
• The ischemic brain fires massive sympathetic signals
• Result: extreme vasoconstriction, BP raised up to 200-250 mm Hg
• Called the "Cushing reflex" when triggered by raised intracranial pressure
• Acts as the body's last-ditch emergency mechanism

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4. Sympathetic Nervous System - Direct Role

1. Vasoconstriction of arterioles and veins → increases TPR and venous return
2. Increased heart rate (positive chronotropy)
3. Increased contractility (positive inotropy) → raises cardiac output

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5. Stress-Relaxation Response (Vascular Mechanism)

• When BP rises suddenly, vessel walls stretch but then relax over minutes
• Blood volume shifts: high BP causes vessels to distend and "store" extra blood
• Helps dampen sudden BP swings
• Acts over minutes to hours

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6. Capillary Fluid Shift

• When arterial pressure rises: fluid shifts from capillaries into interstitium (fluid leaves the blood) → blood volume drops → CO drops → BP returns down
• When arterial pressure falls: fluid shifts from interstitium into capillaries → blood volume increases → BP rises
• Works over minutes to hours

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PART 2: LONG-TERM REGULATION OF BLOOD PRESSURE

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The Golden Principle (Guyton's Concept)

"The kidneys are the ultimate determinants of long-term blood pressure."

• When BP rises → kidneys excrete more Na⁺ and water (urine output increases)
• This reduces blood volume → CO falls → BP returns to normal
• When BP falls → kidneys retain Na⁺ and water → blood volume rises → BP returns up

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1. Renal-Body Fluid Mechanism (Most Important Long-Term Mechanism)

1. BP rises → Glomerular filtration pressure rises
2. Kidneys produce more urine (pressure diuresis + natriuresis)
3. Blood volume decreases
4. Venous return decreases → CO decreases
5. BP returns to normal

• Shift the kidney pressure-output curve to the right (kidneys need higher pressure to excrete the same sodium), OR
• Increase salt and water intake beyond what kidneys can handle

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2. Renin-Angiotensin-Aldosterone System (RAAS)

Low BP / Low Na⁺
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Juxtaglomerular cells release RENIN
        ↓
Renin converts Angiotensinogen → Angiotensin I
        ↓
ACE (in lungs) converts Angiotensin I → Angiotensin II
        ↓
Angiotensin II does THREE things:
1. Vasoconstriction → raises TPR → raises BP
2. Acts on kidneys → increases Na⁺ and water reabsorption → raises blood volume
3. Stimulates adrenal cortex → releases ALDOSTERONE
        ↓
Aldosterone → increases Na⁺ reabsorption in distal tubule and collecting duct
        ↓
Na⁺ retention → water follows → blood volume rises → BP rises

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3. Aldosterone Mechanism (Also Long-Term)

• Aldosterone is a mineralocorticoid from the adrenal cortex
• Acts on kidney tubules to increase Na⁺ reabsorption (and K⁺ excretion)
• More Na⁺ retained → more water retained → blood volume rises → BP rises
• Triggered by: Angiotensin II, high K⁺, low blood volume

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4. ADH (Antidiuretic Hormone / Vasopressin)

• Released from posterior pituitary when BP falls or plasma osmolality rises
• Acts on kidney collecting ducts → retains water → blood volume rises → BP rises
• Also causes vasoconstriction (hence the name vasopressin)
• Works over hours

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5. Atrial Natriuretic Peptide (ANP) - Opposes High BP

• Released from atrial walls when atria are stretched (i.e., when blood volume is high)
• Causes vasodilation and natriuresis (Na⁺ + water excretion in urine)
• Lowers blood volume → lowers BP
• Acts as a counter-regulatory (anti-hypertensive) hormone

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SUMMARY TABLE - Easy Revision

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MEMORY TRICK

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EXAM POINTS (Don't Miss These!)

1. Baroreceptors adapt - they cannot maintain long-term BP control; that's why the kidneys take over.
2. Pressure natriuresis is the kidney's mechanism - the single most important long-term regulator.
3. Angiotensin II has both a direct renal effect AND an aldosterone-mediated effect.
4. ANP opposes the RAAS - it lowers BP by causing salt and water loss.
5. The vasomotor center in the medulla is the CNS headquarters for BP control.
6. Increasing total peripheral resistance alone does NOT permanently raise BP - the kidneys compensate by excreting more fluid, returning BP to normal (unless kidney function is impaired).