regulation of bp
DESCRIPTION
Physiology, CardiovascularTRANSCRIPT
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MEDIUM TO LONG-TERM REGULATION OF BLOOD PRESSURE
Prof Lam Sau Kuen
Department of Physiology
1 2014.11.19 Wed MBBS Stage II UMMP Class of 2013
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Blood Pressure
Pull out, Betty! Pull out! . . . You’ve hit an artery!
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Learning Objectives
• Normal arterial blood pressure (BP)
• Regulation of BP – Short-term regulation of BP
• Baroreceptor reflex • Chemoreceptor reflex • Central nervous system (CNS) ischaemic response
– Medium to long-term regulation of BP
• Renin-angiotensin-aldosterone system (RAAS) • Role of the kidney in long-term regulation
• High BP (hypertension)
– Guidelines
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NORMAL ARTERIAL BP
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Pressure on Vessel Walls
• BP is the lateral pressure exerted by a volume of blood on the walls of the blood vessels as it flows through the vessels
• Arterial BP → BP in aorta and arteries
• Venous BP → BP in veins
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Arterial Blood Pressure
• Systolic and diastolic BP
• Systolic BP (SBP): – 120 mmHg (90 – 130 mmHg) – Highest pressure recorded when
left ventricle is contracting (systole)
– Exerting maximal force on blood
• Diastolic BP (DBP): – 80 mmHg (60 – 90 mmHg) – Lowest pressure recorded when
left ventricle is relaxing (diastole) – Due to elastic recoil and arteriolar
resistance
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Arterial BP
• Normal BP: 120/80 mmHg
• Pulse pressure (PP) • PP = SBP – DBP • PP = 120 – 80 = 40 mmHg
• Mean arterial pressure (MAP)
• MAP = DBP + 1/3 PP • MAP = 80 + 13.3 = 93.3
mmHg (~100 mmHg) • Mean pressure in arteries
during a cardiac cycle • Mean driving force to push
blood through capillaries
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Importance of normal MAP
• To ensure adequate driving force to perfuse tissue
• To prevent extra heavy load on heart (afterload)
• To prevent damage to blood vessels
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Arterial (Systemic) and Pulmonary BP
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• BP is dependent upon:
Cardiac output (CO)
Total peripheral resistance (TPR)
Blood volume
• BP is given by:
BP = CO x TPR
CO = SV X HR
BP = SV X HR X TPR
Changes in SV or HR or TPR or blood volume will alter BP
Each of these factors can be manipulated by drug therapy
Determinants of BP
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Factors Affecting Cardiac Output
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TPR or systemic vascular resistance (SVR):
• Amount of friction against blood flow
• Determined by
– Sympathetic activity
– Diameter of arterioles (resistance vessels)
↓ TPR ↑ TPR
(vasodilation) (vasoconstriction)
TPR
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Summary of Factors affecting BP
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REGULATION OF BP
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Regulation of BP
• Short-term regulation – Fast – Sec-to-sec – “Spurts” – Neural (autonomic reflexes) – Baroreceptor mechanism – Acts by changing CO or TPR – For survival
• Medium to long-term regulation
– Slow – Min-to-min, hour-to-hour, day-to-day, month-to-month, year-to-year – Basal level – Hormonal – Renin-angiotensin-aldosterone system (RAAS) – Involves the kidneys – Acts by regulating blood volume through kidneys
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Short-term Regulation of BP
• Responds within seconds to daily ambulatory changes in BP
• Involves autonomic reflexes • Baroreceptor mechanism
(reflex) (main) • Chemoreceptor reflex • CNS ischaemic response
• Regulates BP by altering CO or TPR
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Baroreceptor Mechanism
Sensory organs: Baroreceptors in carotid sinus + aortic arch
Integrating centre: Cardiovascular centre (CVC) in
medulla
Effector organs: • Heart - SA node - Ventricle • Arterioles
Afferent nerves: • Vagus • Glossopharyngeal
Efferent nerves: • Sympathetic • Parasympathetic
Negative feedback
Stimulus: ↑ or ↓ in BP Response: ↓ or ↑ in BP
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Sensory Organs: Baroreceptors
• Stretch receptors • Respond to blood pressure changes • Located in carotid sinus and aortic arch • Also in large arteries of neck and thorax
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Integrating Centre: Cardiovascular Centre (CVC) in Medulla
CVC
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Effector Organs: Heart and Arterioles
• Sympathetic stimulation:
↑ rate of SA node and conduction
velocity in the AV node
↑ force of contraction of
myocardium
Vaso- and venoconstriction
• Parasympathetic stimulation:
↓ excitability of both SA and AV
node by hyperpolarizing the
membrane during diastole
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Baroreceptor Reflex
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Baroreceptor Reflex: When BP increases
↑ BP: ↑ stretch of baroreceptors → ↑ impulses generated → ↑ impulses to CVC → CVC inhibited → ↓ sympathetic outflow → ↑ parasympathetic outflow → to heart: → ↓ HR, ↓ force of contraction, ↓ SV → ↓ CO → to arterioles: → vasodilation → ↓ TPR BP = SV X HR X TPR → ↓ BP
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Baroreceptor Reflex: Increase in BP
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Baroreceptor Reflex: When BP decreases
↓ BP: ↓ stretch of baroreceptors → ↓ impulses generated → ↓ impulses to CVC → CVC not inhibited → ↑ sympathetic outflow → ↓ parasympathetic outflow → to heart: → ↑ HR, ↑ force of contraction, ↑ SV → ↑ CO → to arterioles: → vasoconstriction → ↑ TPR BP = SV X HR X TPR → ↑ BP
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Baroreceptor Reflex: Decrease in BP
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Chemoreceptor Reflex
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• Chemoreceptors – Carotid bodies – Aortic bodies
• Respond to: – Increase in plasma CO2 (decrease in
pH) • More sensitive
– Decrease in O2
• Less sensitive • Impulse sent to CVC • Increase sympathetic outflow • Increase HR and force of contraction • Increase in CO and hence BP • More blood flows to lungs for removal
of CO2 and intake of O2
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CNS Ischaemic Response
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• Last ditch response to increase BP • Stimulus: MAP < 60 mmHg
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Long-term Regulation of BP
• Medium to long-term regulation – Slow – Min-to-min, hour-to-hour, day-to-
day, month-to-month, year-to-year
– Involves hormonal regulation of blood volume by kidneys
• By controlling water balance – Water intake = water
output – Antidiuretic hormone
(ADH) or arginine vasopressin (AVP)
• By controlling Na+ balance – Na+ intake = Na+ output – RAAS – Natriuretic peptides (NP)
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Water Balance
• AVP • Hormone that regulates ECF fluid
volume • Synthesised in hypothalamus • Stored and released from posterior
pituitary gland • Triggers for secretion
• Hypovolaemia • Hypotension • Extracellular hyperosmolarity • Angiotensin II • Sympathetic stimulation
• Acts on renal collecting ducts via V2 receptors to increase reabsorption of water
• Increases blood volume, CO and hence BP
• Also causes vasoconstriction 30
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Water Balance
• Water intake = water output
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Na+ Balance
• Na+ intake = Na+ output
• Na+ – Most important ECF ion – Most abundant ion – Major determinant of ECF vol – Thus determines BP
• Controlled by RAAS
– Reabsorption of Na+
• Counter-regulated by natriuretice peptides (NP)
– Atrial NP (ANP) from atrial walls – Brain BP (BNP) from ventricular walls – Excretion of Na+
• Handled by kidneys
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Renal Regulation of Blood Pressure
• In the kidney – Juxtaglomerular apparatus (JGA)
• Located in cortex
• Unique segment:
– Thick ascending limb of the loop of Henle passes between the afferent and efferent arterioles of its own glomerulus
• Three special tissues:
– Macula densa – point of contact between ascending limb and arterioles (modified thick aLoH cells)
– JG cells – modified smooth muscle cells of afferent arterioles (granular cells) that synthesise and secrete renin
– Lacis cells (extraglomerular mesangial cells), not granular but also secrete renin
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JGA
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Sensory Receptors in JGA
• Two sensors are present in the JGA
• In macula densa
– Sensory receptors that detect changes in Na+ concentration in tubular fluid of PCT
• In afferent arteriole
– Baroreceptors (stretch receptors) that detect changes in perfusion pressure of arterial blood
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Renal Regulation of Blood Pressure
• Decrease in BP perfusion pressure
• Or Na+ filtered concentration in tubular
fluid
• Results in stimulation of renin secretion from
JG cells
• Renin angiotensin II formation
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Renal Regulation of Blood Pressure
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Renal Regulation of Blood Pressure
• Role of kidneys
– Aldosterone increased Na+ (and water) reabsorption from CD
– Action of ADH on vasopressin receptors (V2) increased water reabsorption from CD
• Result in ECF volume expansion and an increase in BP
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Renal Regulation of Blood Pressure
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Figure 26.9
Maintenance of Blood Pressure Homeostasis
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HYPERTENSION
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Hypertension
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• Guidelines
– WHO-ISH: 140/90 mmHg (MAP 106.7, normal – 93.3, set-point resets)
– JNC-VII: 140/90
• Optimum <120/<80 (115/75 “new” normal)
• >120/>80 now considered to be pre-hypertension – higher risk of developing hypertension
– BHS: 140/90
– Malaysia: 140/90
• Risk is important and in diabetes: 130/80 mmHg
• Two types:
– Primary – cause largely unknown – etiology poorly understood
– Secondary – cause known – due to disease process
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High Blood Pressure: Risk Factors
• Age
• Race
• Heredity (“Bad” genes)
• Diet – high fat and salt
• Stress
• Inactivity
• Obesity
• Smoking
• Alcohol consumption
• Diabetes
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High Blood Pressure: Symptoms
• Silent killer
• Patients are usually asymptomatic until substantial vascular damage occurs
• In more severe cases
– Persistent throbbing headaches
– Blurred vision
– Nausea and vomiting
– Ringing in ears - tinnitus
– Chest pain
– Swollen feet
– Mini-strokes
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Treating Hypertension
Lifestyle
Changes
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Treating Hypertension
CLASSES OF DRUGS MECHANISM OF ACTION
Diuretics Increase urine volume
Beta-blockers Decrease HR
Decrease ventricular contractility
Calcium antagonists/blockers Block Ca2+ channels
Vasodilation
ACE inhibitors Inhibit conversion of angiotensin I to angiotensin II
Vasodilation
Angiotension II-receptor antagonists
Block receptors
Vasodilation
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