1. BLOOD PRESSURE REGULATION:

2. (a) Arterial Baroreceptors
. At its origin from the common carotid artery, the internal carotid artery shows a small dilatation, called the carotid sinus.
The tunica adventitia contains a large number of highly branched, coiled and inter-twined naked nerve endings of myelinated nerve fibers .
These nerve-endings are highly sensitive to distortion or stretch produced by pressure within the artery.

3. LOCATION AND INNERVATION OF ARTERIAL BARORECEPTORS:

4. Determinants of Arterial Blood Pressure:
Cardiac output.
2. Peripheral resistance.
3. Elasticity of the aorta and large
arteries (windkessel vessels).
4. Blood volume.

5. Carotid sinus baroreceptors

7. Pattern of Baroreceptor Discharge
No response to blood pressure below 60 mmHg.
Above this pressure, the discharge rate increases with increase in perfusion pressure, but the response is non-linear.
Baroreceptors are most sensitive around the mean pressure of 100 mm Hg
Beyond 200 mm Hg pressure, there is no further increase in the rate of the discharge in the baroreceptors.

9. Effect of Changes in Baroreceptor Discharge
Increased discharge in baroreceptors
inhibits activity of medullary VMC
increases the vagal discharge to the heart.
Result: vasodilatation (decreased peripheral resistance),
venodilatation,
bradycardia
decreased cardiac output.
The arterial blood pressure falls.

10. Baroreceptors cont
A decrease in the baroreceptor discharge: increased activity of VMC:
vasoconstriction (increased peripheral resistance),
venoconstriction (decreased venous pooling and thus increased venous return),
Increase in heart rate and cardiac output.
The arterial blood pressure increases.

11. Baroreceptor mechanism:

12. Function of Arterial Baroreceptors
Any rise in BP results in greater impulse discharge in the sinus and aortic nerves.
The resultant inhibition of VMC decreases the CO as well as the PR.
As a result BP falls to near normal level .

14. Chemoreceptors
Chemoreceptors in the carotid body and the aortic body respond to changes in pO2, pCO2, and pH of the blood.
These receptors are primarily concerned with the regulation of pulmonary ventilation.
The chemoreceptors have an excitatory action on the VMC.
In severe hypotension produced by hemorrhage, increased chemoreceptor discharge may help to elevate BP.

15. Long Term Arterial Blood Pressure Regulation
The kidneys play a dominant role in this long term regulation of blood pressure by changes in the blood volume (or ECF volume).
The kidneys have an ability to regulate the ECF volume by regulation of salt (NaCl) and water excretion.
In addition, the rennin-angiotensin-aldosterone system helps in the regulation of salt and water excretion by the kidneys.
A failure of this long term regulatory mechanism is responsible for the disorder known as essential hypertension

16. Vaso Construction BP, Blood Flow
CNS ischaemic response:
Blood flow VMC ( Co2) Strong
(BP 60mmHg.) Sympathetic Stimulation
Vaso Construction BP, Blood Flow

17. Arterial Pressure (arteries in the CSF (P) brain compressed)
CUSHING REFLEX ?
Arterial Pressure (arteries in the CSF (P) brain compressed)
Blood supply to Brain
CNS ischaemic response BP

18. Why the baroreceptors do not bring blood pressure back to normal in chronic hypertensive individuals ?
Normal individual having normal blood pressure, the baroreceptors maintain the B. P. within a normal narrow range when there is deviation. However the effects of reflexes do not last long, adaptation and resetting of baroreceptors occur. Thus in hypertensive individuals there is resetting of the baroreceptor reflex mechanism and the receptors try to maintain the B.P. at the new set point or elevated level rather than at normal level.

19. Heart Rate Regulation Cardiac Innervation:
Sympathetic: Positive chronotropic
Positive inotropic effects
Parasympathetic (vagus)
Negative chronotropic
Negative inotropic effects

20. The normal heart rate (range 60–90/min,) mean 75/min.
Tachycardia: heart rate > 90/min
Bradycardia: heart rate < 60/min
Variations in the heart rate can occur by
a change in the vagal discharge and/or
change in sympathetic discharge.
In trained athletes, the resting heart rate is around 60/min, because the athletic training increases the vagal tone.
In maximal athletic activity (or exercise on a treadmill) the heart rate may increase to a value as high as 180–200/min.

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