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Sem Physiol 12 – Nervous
control of circulation and rapid
and long term control of blood
pressure
Prof. dr. Željko Dujić
Figure 18-1 Anatomy of sympathetic nervous control of the circulation. Also shown by the dashed red line, a vagus nerve that carries parasympathetic signals to the
heart.
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Figure 18-2 Sympathetic innervation of the systemic circulation.
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- Sympathetic innervation – T1-L2, innervation of
arterioles – regulation of resistance, innervation of
veins – regulation of bloow volume
- Parasympathetic (vagus) control of the heart –
bradicardia, minimal reduction of the contractility of
the heart
- Sympathetic vasoconstrictor system especially
developed in kidneys, skin, gut, spleen
Figure 18-3 Areas of the brain that play important roles in the nervous regulation of the circulation. The dashed lines represent inhibitory pathways.
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- NTS – afferent signals from periphery
(vagus and glossopharyngeus) primarily heart
and lungs
- Vasomotor center – lateral areas excitation,
medijal areas near dorsal motor nucleus
(vagus) = kardioinhibicija
- Medulla of suprarenal gland, symp.
Vasodilator system (ACH and epinephrine),
vasovagal syncope (fainting due to emotions)
– cardioinhibitory influence
- Stimulation of many areas of the brain
influences cardiovaskular system
Figure 18-4 Effect of total spinal anesthesia on the arterial pressure, showing marked decrease in pressure resulting from loss of "vasomotor tone."
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- Sympathetic activation – vasoconstriction,
venoconstriction, heart excitation, during few
seconds maximal activation is reached
- Stressfull activation “all-or-none” response
- Exercise – despite reduction in TPR, mean
arterial pressure is increased, vasoconstriction
in active and inactive muscles
Figure 18-5 The baroreceptor system for controlling arterial pressure.
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Figure 18-6 Activation of the baroreceptors at different levels of arterial pressure. ΔI, change in carotid sinus nerve impulses per second; ΔP, change in
arterial blood pressure in mm Hg.
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- Baroreceptors react strongest when BP is rapidly
changing, contrary to steady state conditions
- Baroreceptors adaptation – hypertension,
unimportance of baroreceptors in long term control
of BP
- Cardioinhibitory reflex
- Buffer role in every day BP changes from seconds
to seconds (posture change)
Figure 18-9 Frequency distribution curves of the arterial pressure for a 24-hour period in a normal dog and in the same dog several weeks after the baroreceptors had
been denervated. (Redrawn from Cowley AW Jr, Liard JP, Guyton AC: Role of baroreceptor reflex in daily control of arterial blood pressure and other variables in dogs.
Circ Res 32:564, 1973. By permission of the American Heart Association, Inc.)
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- Control of BP by carotid and aortal
chemoreceptors (mean BP fall below
80mmHg) – chemo and baroreceptors role
- Atrial reflexes, volume reflex, ANP, ADH
decrease, reduction of sympathetic tone,
reduction in colloid osmotic plasma pressure
- Bainbridge’s reflex – reflex increase in HR,
direkt expansion (increased frequency for 4060%)
- Ischemic CNS reaction – reduced BP below 60 mmHg,
increased intracranial CSF pressure (Cushing’s reaction)
- Abdominal wall compression reflex, paralyzed patients,
increased intraabdominal pressure, compression of IVC
(inferior vena cava)
- Compression of skeletal muscle blood vessels centralizes
blood from large perypheral veins towards heart (central
compartment of the cardiovascular system)
- Spleen, translocation of blood from large veins and
intraabdominal organs such as liver, importance of
sympathetic activation, splenic capsular contraction, respons
within seconds
- Respiratory waves in BP (invasively
measured) (mixing signals between
respiratory and vasomotor centers in the pons
and medulla), increased BP at the start of deep
inspiration, reduction in other phases of the
respiratory cycle
- “Vasomotor” waves in BP – oscillation of
the reflex control systems (Meyer’s waves) –
baroreceptors, chemorecepts, ishemic reaction
of CNS
- Dominant role of kidney in long term BP
regulation (infinite gain, no error!!)
- Pressure diuresis curve, natriuresis
(measured also on the isolated and perfused
kidney!!)
- BP regulation in animals with inactivated
baroreceptors - dennervation
- Infinite gain of kidney – body fluids in long
term BP regulation
- ABP = CO x TPR (total peripheral
resistance)
- If TPR is increased but without change in
renaln artery MAP is unchanged due to
dominant effect of pressure diuresis
- Renal disease and hypertension
- Hardly measured increased in CO results in
large increase in TPR with consequent
hipertension
- Increased salt intake does not increases BP if
kidney work normally
- Compensatory mechanism of extra
morphology and function in kidneys (80-90%
reserve)
- Hypertension in primary aldosteronism
- Renin remains in circulation for 30-60 min
- A II remains 1-2 min
- Full activation of renin-AII system within 20
min, mid-term BP regulation
- AII stimulates aldosterone secretion, thirst
center, reapsorption of sodium in proximal
tubule (kidney)
- ACE inhibitors
-Goldblatt
hypertension with one or two
kidneys, renin-dependent hypertension
(secondary hypertension, known cause –
kidney disease)
- Aortic coarctation (increased pressure in the
upper parts of the body above coarctation and
normal pressure in lower parts of the body)
- Rapid mechanisms: baro, chemoreceptors
and ischemic CNS reaction (seconds)
- Medium fast or mid term: stress-relaxation,
capillary fluid shift, renin-AII-aldo system
(30-60 minutes)
- Long term: kidney (2-3 days)