1. Regulation of circulation and blood pressure overview

2. Regulation of circulation and BP
Nervous control
Renal-body fluid system
Renin-angiotensin
Aldosterone
ADH

3. OUTLINE OF NERVOUS CONTROL OF CVS

4. Nervous control is through Autonomic Nervous System (ANS)
ANS has two parts
Sympathetic (mainly controls blood vessels)
Parasympathetic (mainly controls heart)

5. Physiologic anatomy of sympathetic system
Sympathetic vasomotor nerve fibers leave the spinal cord through all the thoracic spinal nerves and through the first one or two lumbar spinal nerves.
They then pass immediately into a sympathetic chain, one of which lies on each side of the vertebral column. Next, they pass by two routes to the circulation:
(1) through specific sympathetic nerves that innervate mainly the vasculature of the internal viscera and the heart,
(2) almost immediately into peripheral portions of the spinal nerves distributed to the vasculature of the peripheral areas

11. Sympathetic innervation of blood vessels
All vessels except capillaries are innervated
Very little innervation of metarterioles and precapillary sphincters
Rich innervation of arterioles, small arteries
Innervation of veins
Innervation of heart

12. Effect of sympathetic stimulation
Increased heart rate
Increased force of contraction
Constriction of arterioles
Constriction of veins
Increased release of adrenaline by adrenal medulla
Increased renin release by kidneys

13. Neurotransmitter of sympathetic nerve endings at most areas is noradrenaline
Adrenal medulla produces adrenaline and nor adrenaline

14. In skeletal blood vessels
Nor epinephrine causes vasoconstriction
Epinephrine causes vasodilation
Metabolic control is the most effective way

15. Parasympathetic innervation
It is through vagus nerve to heart
It decreases heart rate
Slightly decreases contractility of heart

16. Vasomotor area
Vasomotor area is located in lower pons and medulla bilaterally
It sends parasympathetic impulses to heart through vagus
It sends sympathetic impulses through spinal cord

19. Important parts of vasomotor center
Vasoconstrictor area located bilaterally in anterolateral part of upper medulla
Vasodilator area located bilaterally in anterolateral part of lower medulla
Sensory area called Tractus solitarius located bilaterally in posterlateral part of medulla and lower pons

20. Control of heart by vasomotor center
Lateral part increases heart rate
Medial part decreases heart rate through vagus

21. Control of vasomotor center by higher centers of CNS
Hypothalamus (Posterior part is excitatory, anterior is inhibitory)
Reticular substance of pons, midbrain, diencephalon
Limbic system
Motor areas of cerebral cortex

22. Vasomotor tone
In resting state vasoconstrictor area of vasomotor center sends excitatory signals to spinal cord
Which sends excitatory signals to blood vessels
These impulses maintain baseline contraction of smooth muscles of blood vessels
This baseline sympathetic discharge maintaining smooth muscle contraction of blood vessels is called vasomotor tone

23. Vasovagal syncope
Fainting due to disturbed emotional thoughts in cerebral cortex
From cerebral cortex to anterior hypothalamus
Stimulation of vagus nerve
Activation of vasodilator sympathetic fibers of skeletal muscles
Pooling of blood in vessels of muscles

24. Vasodilatation of skeletal vessels
Fall in BP
Decreased heart rate
Brain is deprived of blood flow
Person faints

25. Control of BP through nervous system
How sympathetic system increases BP
Constriction of arterioles
Constriction of veins
Stimulation of heart

26. Reflex mechanisms for maintaining BP
Baroreceptor
Chemoreceptors
Low pressure receptors(volume reflex, Inc H.R)
CNS ischemic response
Abdominal compression reflex

27. Baroreceptor reflex

32. Components of baroreceptor reflex
Afferent
Center
Efferent
Effectors

33. Receptors Baroreceptors (Nerve endings) located in
carotid sinus present in internal carotid artery
Aortic arch
Also present in few great vessels of neck and thorax
These receptors are excited by stretch due to increase in BP (60-180)

34. Center Integration occurs at vasomotor center
Sensory input is received at Tractus solitarius in medulla and lower pons
From TS impulses go to vasoconstrictor area and to vagus nerve nucleus.

35. Efferents Vagus nerve resulting in slowing of heart
Decreased activity of sympathetic nerves arising from vasomotor center resulting in less constriction of vessels and decreased cardiac activity
Long term rise in BP also decreases sympathetic activity in kidneys

36. Effectors
Heart
Blood vessels
kidneys

37. When person stands from lying position
When a person goes from supine to an upright posture, the following important changes take place:
Pressure in the dependent veins increases.
Blood volume in the dependent veins increases.
Circulating blood volume (cardiac output) decreases.
Blood pressure decreases in upper half.
Compensation via the carotid sinus reflex will include:
Total peripheral resistance increases.
Heart rate increases.
The changes induced by the carotid sinus returns blood pressure toward the value in the supine position, but in cases compensation will not be complete.

39. Chemoreceptor reflex

40. Receptors
Receptors are Chemoreceptors which are present in aortic bodies and carotid bodies (common carotid arteries)
Stimulated by rise in H ions and CO2 , and fall in O2
Stimulated by BP below 80 mm of Hg

42. Afferents
From carotid bodies impulses are conducted through Hering’s nerve to glossopharyngeal nerve to Tractus solitarius
From aortic arch impulses are conducted through vagus nerve to tractus solitarius

43. Center and effectors
Integration occurs at Vasomotor center and respiratory center
If BP falls rise in BP by vaso-constriction
Stimulation of respiratory center

44. Atrial reflexes Bainbridge reflex (control of heart rate)
Stimulation of SA node (control of heart rate)
Atrial volume reflexes that
activate the kidneys (dilation of arterioles of kidneys and decreased secretion of ADH)
Increased production of ANP

46. Bainbridge reflex
This reflex is initiated when the nerve endings in the wall of the right atrium are stimulated by a rise of venous pressure.
The afferent fibers ascend in the vagus to the medulla oblongata and terminate on the nucleus of the tractus solitarius .
Connector neurons inhibit the parasympathetic nucleus (dorsal) of the vagus, and sympathetic fibers stimulate the cardiac activity.

47. CNS Ischemic response
The arterial pressure elevation in response to cerebral ischemia is known as CNS ischemic response. (very powerful response)
The response becomes significant when arterial pressure falls below 60 mm of mercury.
Maximum stimulation occurs at pressure of 15 to 20 mm of mercury

50. There is decreased blood flow to Vasomotor area
Build up of CO2, lactic acid and other acidic substances in vasomotor center
Due to CNS ischemic response blood pressure can rise up to 250 mm of mercury.

51. Due to this response BP rises as a result of intense sympathetic vasoconstriction of peripheral vessels

52. Cushing reaction
This is CNS ischemic response due to rise in CSF pressure around the brain in cranial vault
Cushing reaction protects vital centers of the brain from loss of nutrition, when CSF pressure becomes more than the arterial BP

54. Abdominal compression reflex
Contraction of abdominal muscles
Compression of blood vessels
Increased venous return

55. Effect of respiration on BP
In inspiration systolic BP falls by 10 mm of mercury
In deep breathing this fall is about 20 mm of mercury
During inspiration Pulmonary veins retain blood due to negative intrathoracic pressure and venous return to left atrium decreases and left ventricular output falls

56. Kidney-body fluid mechanisms
Direct method
Pressure diuresis
Pressure natriuresis
This is regulated by
increase or decrease in BP
Intake of salt and water
At BP of 50 no urine output, at 100 normal output, at 200, 6-8 times normal

57. When renal artery BP INCREASE
Reduction in water and sodium resorption in proximal tubule
Increased BP  --> Increased peritubular capillary pressure  --> Increased renal interstitial pressure  --> Decreased fluid and sodium absorption
Angiotensin II and sympathetic activity
When BP increase, both angiotensin II and sympathetic activities decrease.
Direct little increase in GFR

59. Control through renin angiotensin system

61. Actions of angiotensin 11
Acts directly on kidneys
Causes release of Aldosterone
Causes vasoconstriction
Increases thirst

62. Components of renin-angiotensin system
Renin stored as prorenin in JG cells of kidneys
JG cells are smooth muscle cells of afferent arterioles
Fall in BP causes release of renin from JG cells
Renin converts angiotensinogen to angiotensin1
Angiotensin 1 is converted to angiotensin11 predominantly in the lungs by ACE

65. Renin-Angiotensin system is an effective feedback mechanism for regulating blood pressure

66. How increased salt intake is balanced in healthy subjects

67. Nervous mechsnisms, diuresis through kidneys and Renin-Angiotensin system if functioning properly are efficient mechanisms for preventing sudden change in BP
If mechanisms are proper (Salt insensitive)
If mechanisms not proper (Salt sensitive)

68. Regulation of blood pressure
Rapidly Acting Pressure Control Mechanisms, Acting Within Seconds or Minutes
Pressure Control Mechanisms That Act After Many Minutes
Long-Term Mechanisms for Arterial Pressure Regulation.

70. Rapidly Acting Pressure Control Mechanisms, Acting Within Seconds or Minutes
The Baroreceptor mechanism
CNS ischemic response
The Chemoreceptor mechanism

71. Pressure control mechanisms that act after many minutes
These mechanisms start within 30 minutes to several hours
Renin-angiotensin vasoconstrictor mechanism
Stress relaxation of vasculature
Fluid shift through capillary walls in and out of circulation

72. Long term mechanisms for arterial pressure regulation
Secretion of Aldosterone
Secretion of ADH