1. Sem Physiol 12 – Nervous control of circulation and rapid and long term control of blood pressure
Prof. dr. Željko Dujić

2. Figure 18-1 Anatomy of sympathetic nervous control of the circulation
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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3. Figure 18-2 Sympathetic innervation of the systemic circulation.
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4. - 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

5. 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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6. - 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

7. 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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8. - 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

9. Figure 18-5 The baroreceptor system for controlling arterial pressure.
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10. 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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11. - 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)

14. 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, By permission of the American Heart Association, Inc.)
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15. - 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 40-60%)

17. - 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

19. - 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

20. - 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

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

26. - 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

31. - 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

33. - 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

38. 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)

41. - 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)