Sem Physiol 12 – Nervous Sem Physiol 12 – Nervous control of circulation and rapid control of circulation and rapid and long term control of blood and long term control of blood

pressure pressure

Prof. dr. Željko DujićProf. 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 - Sympathetic innervation – T1-L2, innervation of arterioles – regulation of resistance, innervation of arterioles – regulation of resistance, innervation of veins – regulation of bloow volumeveins – regulation of bloow volume

- Parasympathetic (vagus) control of the heart – - Parasympathetic (vagus) control of the heart – bradicardia, minimal reduction of the contractility of bradicardia, minimal reduction of the contractility of the heartthe heart

- Sympathetic vasoconstrictor system especially - Sympathetic vasoconstrictor system especially developed in kidneys, skin, gut, spleen 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 - NTS – afferent signals from periphery (vagus and glossopharyngeus) primarily heart (vagus and glossopharyngeus) primarily heart and lungsand lungs- Vasomotor center – lateral areas excitation, - Vasomotor center – lateral areas excitation, medijal areas near dorsal motor nucleus medijal areas near dorsal motor nucleus (vagus) = kardioinhibicija(vagus) = kardioinhibicija- Medulla of suprarenal gland, symp. - Medulla of suprarenal gland, symp. Vasodilator system (ACH and epinephrine), Vasodilator system (ACH and epinephrine), vasovagal syncope (fainting due to emotions) vasovagal syncope (fainting due to emotions) – cardioinhibitory influence– cardioinhibitory influence- Stimulation of many areas of the brain - Stimulation of many areas of the brain influences cardiovaskular system 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, - Sympathetic activation – vasoconstriction, venoconstriction, heart excitation, during few venoconstriction, heart excitation, during few seconds maximal activation is reachedseconds maximal activation is reached

- Stressfull activation “all-or-none” response- Stressfull activation “all-or-none” response

- Exercise – despite reduction in TPR, mean - Exercise – despite reduction in TPR, mean arterial pressure is increased, vasoconstriction arterial pressure is increased, vasoconstriction in active and inactive musclesin 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 - Baroreceptors react strongest when BP is rapidly changing, contrary to steady state conditionschanging, contrary to steady state conditions

- Baroreceptors adaptation – hypertension, - Baroreceptors adaptation – hypertension, unimportance of baroreceptors in long term control unimportance of baroreceptors in long term control of BPof BP

- Cardioinhibitory reflex- Cardioinhibitory reflex

- Buffer role in every day BP changes from seconds - Buffer role in every day BP changes from seconds to seconds (posture change)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 - Control of BP by carotid and aortal chemoreceptors (mean BP fall below chemoreceptors (mean BP fall below 80mmHg) – chemo and baroreceptors role80mmHg) – chemo and baroreceptors role

- Atrial reflexes, volume reflex, ANP, ADH - Atrial reflexes, volume reflex, ANP, ADH decrease, reduction of sympathetic tone, decrease, reduction of sympathetic tone, reduction in colloid osmotic plasma pressure reduction in colloid osmotic plasma pressure

- Bainbridge’s reflex – reflex increase in HR, - Bainbridge’s reflex – reflex increase in HR, direkt expansion (increased frequency for 40-direkt expansion (increased frequency for 40-60%)60%)

- Ischemic CNS reaction – reduced BP below 60 mmHg, - Ischemic CNS reaction – reduced BP below 60 mmHg, increased intracranial CSF pressure (Cushing’s reaction)increased intracranial CSF pressure (Cushing’s reaction)

- Abdominal wall compression reflex, paralyzed patients, - Abdominal wall compression reflex, paralyzed patients, increased intraabdominal pressure, compression of IVC increased intraabdominal pressure, compression of IVC (inferior vena cava)(inferior vena cava)

- Compression of skeletal muscle blood vessels centralizes - Compression of skeletal muscle blood vessels centralizes blood from large perypheral veins towards heart (central blood from large perypheral veins towards heart (central compartment of the cardiovascular system)compartment of the cardiovascular system)

- Spleen, translocation of blood from large veins and - Spleen, translocation of blood from large veins and intraabdominal organs such as liver, importance of intraabdominal organs such as liver, importance of sympathetic activation, splenic capsular contraction, respons sympathetic activation, splenic capsular contraction, respons within secondswithin seconds

- Respiratory waves in BP (invasively - Respiratory waves in BP (invasively measured) (mixing signals between measured) (mixing signals between respiratory and vasomotor centers in the pons respiratory and vasomotor centers in the pons and medulla), increased BP at the start of deep and medulla), increased BP at the start of deep inspiration, reduction in other phases of the inspiration, reduction in other phases of the respiratory cyclerespiratory cycle

- “Vasomotor” waves in BP – oscillation of - “Vasomotor” waves in BP – oscillation of the reflex control systems (Meyer’s waves) – the reflex control systems (Meyer’s waves) – baroreceptors, chemorecepts, ishemic reaction baroreceptors, chemorecepts, ishemic reaction of CNSof CNS

- Dominant role of kidney in long term BP - Dominant role of kidney in long term BP regulation (infinite gain, no error!!)regulation (infinite gain, no error!!)

- Pressure diuresis curve, natriuresis - Pressure diuresis curve, natriuresis (measured also on the isolated and perfused (measured also on the isolated and perfused kidney!!)kidney!!)

- BP regulation in animals with inactivated - BP regulation in animals with inactivated baroreceptors - dennervationbaroreceptors - dennervation

- Infinite gain of kidney – body fluids in long - Infinite gain of kidney – body fluids in long term BP regulationterm BP regulation

- ABP = CO x TPR (total peripheral - ABP = CO x TPR (total peripheral resistance) resistance)

- If TPR is increased but without change in - If TPR is increased but without change in renaln artery MAP is unchanged due to renaln artery MAP is unchanged due to dominant effect of pressure diuresisdominant effect of pressure diuresis

- Renal disease and hypertension- Renal disease and hypertension

- Hardly measured increased in CO results in - Hardly measured increased in CO results in large increase in TPR with consequent large increase in TPR with consequent hipertensionhipertension

- Increased salt intake does not increases BP if - Increased salt intake does not increases BP if kidney work normallykidney work normally

- Compensatory mechanism of extra - Compensatory mechanism of extra morphology and function in kidneys (80-90% morphology and function in kidneys (80-90% reserve)reserve)

- Hypertension in primary aldosteronism- Hypertension in primary aldosteronism

- Renin remains in circulation for 30-60 min- Renin remains in circulation for 30-60 min

- A II remains 1-2 min- A II remains 1-2 min

- Full activation of renin-AII system within 20 - Full activation of renin-AII system within 20 min, mid-term BP regulation min, mid-term BP regulation

- AII stimulates aldosterone secretion, thirst - AII stimulates aldosterone secretion, thirst center, reapsorption of sodium in proximal center, reapsorption of sodium in proximal tubule (kidney)tubule (kidney)

- ACE inhibitors- ACE inhibitors

-Goldblatt hypertension with one or two Goldblatt hypertension with one or two kidneys, renin-dependent hypertension kidneys, renin-dependent hypertension ((secondary hypertensionsecondary hypertension, known cause – , known cause – kidney disease)kidney disease)

- Aortic coarctation (increased pressure in the - Aortic coarctation (increased pressure in the upper parts of the body above coarctation and upper parts of the body above coarctation and normal pressure in lower parts of the body)normal pressure in lower parts of the body)

- Rapid mechanisms: baro, chemoreceptors - Rapid mechanisms: baro, chemoreceptors and ischemic CNS reaction (and ischemic CNS reaction (secondsseconds))

- Medium fast or mid term: stress-relaxation, - Medium fast or mid term: stress-relaxation, capillary fluid shift, renin-AII-aldo system capillary fluid shift, renin-AII-aldo system ((30-60 minutes30-60 minutes))

- Long term: kidney (- Long term: kidney (2-3 days2-3 days))