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BLOOD PRESSURE-NEURAL AND
CHEMICAL REGULATION
BY,
S.HARSRITHA
(17BIOB07)
BLOOD PRESSURE
Arterial blood pressure can be defined as the lateral pressure
exerted by the moving column of blood on the walls of the arteries.
measured as mmHg.
Changes in pressure are the driving force that moves blood through
the circulatory system.
SIGNIFICANCE
 To ensure the blood flow to various organs.
 Plays an important role in exchange of nutrients and gases
across the capillaries.
 Required to form urine.
 Required for the formation of the lymph.
NORMAL VALUES
 Normal Adult range
Can fluctuate within a
wide range and still
be normal
Systolic/diastolic
100/60 - 140/80
Normal Adult range
Can fluctuate within a
wide range and still
be normal
Systolic/diastolic
100/60 - 140/80
 The maximum pressure during
ventricular contraction is called
the systolic pressure. Normal
range (90-140 mm Hg).
 The lowest pressure that
remains in the arteries before
the next ventricular contraction
is called the diastolic pressure.
Normal range (60 -90 mm
Hg).
Arterial blood pressure rises and falls according to cardiac cycle
phases.
 Pulse pressure is a measure of
the strength of the pressure
wave.
 Denotes the difference between
systolic and diastolic pressure.
 Mean arterial pressure is estimated as diastolic pressure
plus one-third of pulse pressure.
 Mean arterial pressure is closer to diastolic pressure
than to systolic pressure because diastole lasts twice as
long as systole.
 Mean arterial pressure (MAP) is a function of cardiac output
and resistance in the arterioles (peripheral resistance).
 The cardiac output is defined as the volume discharged from the
ventricle per minute.
 Peripheral resistance defined as the resistance to flow offered by
the arterioles
BP = Cardiac output X PR
FACTORS MAINTAINING BLOOD PRESSURE
 Cardiac output (CO= SV X PR)
 Circulating blood volume
(This mainly affects systolic B.P)
 Elasticity of the vessel wall
 Peripheral resistance.
RECORDING OF
BLOOD PRESSURE
 Palpatory method
 Auscultatory method
 PALPATORY METHOD which records the pressure at
which the subject feels the first pulse in the artery.
 The detected pressure is systolic pressure.
MEASUREMENT DEVICE
Automated bp device
Aneroid
sphygmomanometer Simple mercury
sphygmomanometer
 AUSCULTATORY METHOD in which the researcher detects the pulse by
listening via a stethoscope placed in the antecubital fossa over the brachial
artery.
 When the cuff pressure is higher than the systolic pressure, no sound is to be
heard.
 The pressure at which the first sound is heard is the systolic pressure, at which
the blood flow resumes and is turbulent.
 As the cuff pressure continues to drop, the sound becomes muffler and finally
disappears.
 The pressure at which the sound disappears was the considered the diastolic
pressure
PRINCIPLE INVOLVED IN RECORDING BLOOD PRESSURE
HYPERTENSION:
High blood pressure, clinically
diagnosed when above 140/90
mmHg.
HYPOTENSION:
Low blood pressure, clinically
diagnosed when below 100/60
mmHg.
REGULATION OF
BLOOD PRESSURE
SHORT TERM
BARO RECEPTOR
REFLEX
HORMONES
CHEMORECEPTOR
REFLEX
LONG TERM
RENIN
ANGIOTENSIN
ALDOSTERONE
SYSTEM
NEURAL REGULATION
REGULATION OF BLOOD PRESSURE
 Achieved through the role of cardiovascular centers
located in the medulla oblongata and baroreceptor
stimulation
 This cluster of neurons responds to changes in
blood pressure as well as blood concentrations of
oxygen, carbon dioxide, and other factors such as
pH.
 Baroreceptor: A nerve ending that is sensitive to
changes in blood pressure.
CARDIO ACCELATORY CENTRE
• SYMPATHETIC
CARDIO INHIBITORY CENTRE
• PARASYMPATHETIC
CARDIAC CENTER
 Autonomic control of heart
VASOMOTOR CENTER
 Autonomic control of blood vessels
 Stimulation of vasomotor
center:VASOCONSTICTION
 Inhibition of vasomotor
center: VASODILATION
BARORECEPTOR FUNCTION  Receptors located within thin areas
of blood vessels and heart chambers
that respond to the degree of stretch
caused by the presence of blood.
 Send impulses to the cardiovascular
center to regulate blood pressure.
 Vascular baroreceptors are found
primarily in sinuses (small cavities)
within the aorta and carotid arteries.
 The aortic sinuses are found in the
walls of the ascending aorta just
superior to the aortic valve, whereas
the carotid sinuses are located in the
base of the internal carotid arteries.
BARORECEPTOR
REFLEXES
CHEMICAL REGULATION
Dilation or constriction of the blood vessels by vasodilators and vasocontrictors.
CHEMICAL VASOCONSTRICTION
Increased concentration of calcium (Ca2+ ions) and phosphorylated
myosin within vascular smooth muscle cells.
A signal transduction cascade leads to increased intracellular calcium
from the sarcoplasmic reticulum through IP3 mediated calcium
release.
Enhances calcium entry across the sarcolemma through calcium
channels.
The rise in intracellular calcium interacts with calmodulin, which in
turn activates myosin light chain kinase.
This enzyme is responsible for phosphorylating the light chain of myosin to
stimulate cross-bridge cycling.
Once elevated, the intracellular calcium concentration is returned to its basal
level through a variety of protein pumps and calcium exchanges located on
the plasma membrane and sarcoplasmic reticulum.
This reduction in calcium removes the stimulus necessary for contraction
allowing for a return to baseline.
Endogenous vasoconstrictors include ATP, epinephrine, and angiotensin II.
Vasodilation is modulated by calcium ion concentration and myosin
phosphorylation within vascular smooth muscle cells.
Dephosphorylation by myosin light-chain phosphatase and induction of calcium
symporters and antiporters that pump calcium ions out of the intracellular
compartment both contribute to smooth muscle cell relaxation and therefore
vasodilation.
This is accomplished through reuptake of ions into the sarcoplasmic reticulum via
exchangers and expulsion across the plasma membrane.
Endogenous vasodilators include arginine and lactic acid.
CHEMICAL VASODILATION
HORMONAL REGULATION
 EPINEPHRINE
 NOR
EPINEPHRINE
ANTIDIURETIC HORMONE: VASOPRESSIN
 Increased release by
posterior pituitary gland in
response to decreased
blood pressure and
decreased blood volume.
 Promotes water
reabsorption by kidneys
 Vasoconstriction of vessels
RENAL REGULATION
 When blood volume is low, renin, excreted by the kidneys, stimulates
production of angiotensin I, which is converted into angiotensin II. This
substance has many effects, including increase in blood pressure due to
its vasoconstrictive properties.
 The cells that excrete renin are called juxtaglomerular cells. When blood
volume is low, juxtaglomerular cells in the kidneys secrete renin directly
into circulation. Plasma renin then carries out the conversion of
angiotensinogen released by the liver to angiotensin I.
 Aldosterone secretion from the adrenal cortex is induced by angiotensin
II and causes the tubules of the kidneys to increase the reabsorption of
sodium and water into the blood, thereby increasing blood volume and
blood pressure.
RENIN ANGIOTENSIN ALDOSTERONE SYSTEM
REFERENCES:
 Rodney Rhoades, David R. Bell Medical
Physiology: Principles for Clinical Medicine.
 http://www.interactive-biology.com/4301/blood-
pressure-short-term-and-long-term-control-
measures/
 Boundless Anatomy and Physiology
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Blood pressure and its regulation

  • 1. BLOOD PRESSURE-NEURAL AND CHEMICAL REGULATION BY, S.HARSRITHA (17BIOB07)
  • 2. BLOOD PRESSURE Arterial blood pressure can be defined as the lateral pressure exerted by the moving column of blood on the walls of the arteries. measured as mmHg. Changes in pressure are the driving force that moves blood through the circulatory system.
  • 3. SIGNIFICANCE  To ensure the blood flow to various organs.  Plays an important role in exchange of nutrients and gases across the capillaries.  Required to form urine.  Required for the formation of the lymph.
  • 4. NORMAL VALUES  Normal Adult range Can fluctuate within a wide range and still be normal Systolic/diastolic 100/60 - 140/80
  • 5. Normal Adult range Can fluctuate within a wide range and still be normal Systolic/diastolic 100/60 - 140/80  The maximum pressure during ventricular contraction is called the systolic pressure. Normal range (90-140 mm Hg).  The lowest pressure that remains in the arteries before the next ventricular contraction is called the diastolic pressure. Normal range (60 -90 mm Hg). Arterial blood pressure rises and falls according to cardiac cycle phases.
  • 6.  Pulse pressure is a measure of the strength of the pressure wave.  Denotes the difference between systolic and diastolic pressure.
  • 7.  Mean arterial pressure is estimated as diastolic pressure plus one-third of pulse pressure.  Mean arterial pressure is closer to diastolic pressure than to systolic pressure because diastole lasts twice as long as systole.
  • 8.  Mean arterial pressure (MAP) is a function of cardiac output and resistance in the arterioles (peripheral resistance).  The cardiac output is defined as the volume discharged from the ventricle per minute.  Peripheral resistance defined as the resistance to flow offered by the arterioles BP = Cardiac output X PR
  • 9. FACTORS MAINTAINING BLOOD PRESSURE  Cardiac output (CO= SV X PR)  Circulating blood volume (This mainly affects systolic B.P)  Elasticity of the vessel wall  Peripheral resistance.
  • 10. RECORDING OF BLOOD PRESSURE  Palpatory method  Auscultatory method  PALPATORY METHOD which records the pressure at which the subject feels the first pulse in the artery.  The detected pressure is systolic pressure.
  • 11. MEASUREMENT DEVICE Automated bp device Aneroid sphygmomanometer Simple mercury sphygmomanometer
  • 12.  AUSCULTATORY METHOD in which the researcher detects the pulse by listening via a stethoscope placed in the antecubital fossa over the brachial artery.  When the cuff pressure is higher than the systolic pressure, no sound is to be heard.  The pressure at which the first sound is heard is the systolic pressure, at which the blood flow resumes and is turbulent.  As the cuff pressure continues to drop, the sound becomes muffler and finally disappears.  The pressure at which the sound disappears was the considered the diastolic pressure
  • 13. PRINCIPLE INVOLVED IN RECORDING BLOOD PRESSURE
  • 14. HYPERTENSION: High blood pressure, clinically diagnosed when above 140/90 mmHg. HYPOTENSION: Low blood pressure, clinically diagnosed when below 100/60 mmHg.
  • 15. REGULATION OF BLOOD PRESSURE SHORT TERM BARO RECEPTOR REFLEX HORMONES CHEMORECEPTOR REFLEX LONG TERM RENIN ANGIOTENSIN ALDOSTERONE SYSTEM
  • 16. NEURAL REGULATION REGULATION OF BLOOD PRESSURE  Achieved through the role of cardiovascular centers located in the medulla oblongata and baroreceptor stimulation  This cluster of neurons responds to changes in blood pressure as well as blood concentrations of oxygen, carbon dioxide, and other factors such as pH.  Baroreceptor: A nerve ending that is sensitive to changes in blood pressure.
  • 17. CARDIO ACCELATORY CENTRE • SYMPATHETIC CARDIO INHIBITORY CENTRE • PARASYMPATHETIC CARDIAC CENTER  Autonomic control of heart
  • 18. VASOMOTOR CENTER  Autonomic control of blood vessels  Stimulation of vasomotor center:VASOCONSTICTION  Inhibition of vasomotor center: VASODILATION
  • 19. BARORECEPTOR FUNCTION  Receptors located within thin areas of blood vessels and heart chambers that respond to the degree of stretch caused by the presence of blood.  Send impulses to the cardiovascular center to regulate blood pressure.  Vascular baroreceptors are found primarily in sinuses (small cavities) within the aorta and carotid arteries.  The aortic sinuses are found in the walls of the ascending aorta just superior to the aortic valve, whereas the carotid sinuses are located in the base of the internal carotid arteries.
  • 21.
  • 22. CHEMICAL REGULATION Dilation or constriction of the blood vessels by vasodilators and vasocontrictors.
  • 23. CHEMICAL VASOCONSTRICTION Increased concentration of calcium (Ca2+ ions) and phosphorylated myosin within vascular smooth muscle cells. A signal transduction cascade leads to increased intracellular calcium from the sarcoplasmic reticulum through IP3 mediated calcium release. Enhances calcium entry across the sarcolemma through calcium channels. The rise in intracellular calcium interacts with calmodulin, which in turn activates myosin light chain kinase.
  • 24. This enzyme is responsible for phosphorylating the light chain of myosin to stimulate cross-bridge cycling. Once elevated, the intracellular calcium concentration is returned to its basal level through a variety of protein pumps and calcium exchanges located on the plasma membrane and sarcoplasmic reticulum. This reduction in calcium removes the stimulus necessary for contraction allowing for a return to baseline. Endogenous vasoconstrictors include ATP, epinephrine, and angiotensin II.
  • 25. Vasodilation is modulated by calcium ion concentration and myosin phosphorylation within vascular smooth muscle cells. Dephosphorylation by myosin light-chain phosphatase and induction of calcium symporters and antiporters that pump calcium ions out of the intracellular compartment both contribute to smooth muscle cell relaxation and therefore vasodilation. This is accomplished through reuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane. Endogenous vasodilators include arginine and lactic acid. CHEMICAL VASODILATION
  • 27.
  • 28. ANTIDIURETIC HORMONE: VASOPRESSIN  Increased release by posterior pituitary gland in response to decreased blood pressure and decreased blood volume.  Promotes water reabsorption by kidneys  Vasoconstriction of vessels
  • 29. RENAL REGULATION  When blood volume is low, renin, excreted by the kidneys, stimulates production of angiotensin I, which is converted into angiotensin II. This substance has many effects, including increase in blood pressure due to its vasoconstrictive properties.  The cells that excrete renin are called juxtaglomerular cells. When blood volume is low, juxtaglomerular cells in the kidneys secrete renin directly into circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I.  Aldosterone secretion from the adrenal cortex is induced by angiotensin II and causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood, thereby increasing blood volume and blood pressure.
  • 31. REFERENCES:  Rodney Rhoades, David R. Bell Medical Physiology: Principles for Clinical Medicine.  http://www.interactive-biology.com/4301/blood- pressure-short-term-and-long-term-control- measures/  Boundless Anatomy and Physiology