REGULATION OF BLOOD PRESSURE

PRESENTED BY Click to edit Master subtitle style NIVIA M 1 st YEAR PG ORAL PATHOLOGY

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Arterial Blood Pressure (BP)

The lateral pressure force generated by the pumping action of the heart on the wall of aorta & arterial blood vessels per unit area. OR = Pressure inside big arteries (aorta & big vessels). Measured in (mmHg), & sometimes in (cmH2O), where1 mmHg = 1.36 cmH2O. Of 2 components:

systolic (= max press reached) = 110-130 mmHg. diastolic (= min press reached) = 70-90 mmHg.
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Arterial Blood Pressure (BP)

Diastolic pressure is more important, because diastolic period is longer than the systolic period in the cardiac cycle.

Pulse pressure = Systolic BP Diastolic BP. Mean arterial pressure = Diastolic BP +

1/3 Pulse pressure.

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Factors affecting Arterial BP

Sex M > F due to hormones/ equal at

menopause. Age Elderly > children due to atherosclerosis. Emotions due to secretion of adrenaline & noradrenaline. Exercise due to venous return. Hormones (e.g. Adrenaline, noradrenaline, thyroid H). Gravity Lower limbs > upper limbs. Sleep due to venous return.
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Blood Pressure = Cardiac Output X Peripheral Resistance

BP depends on:

1. Cardiac output Stroke Volume X Heart Rate =70 ml 72min =5l/min

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Regulation of Arterial Blood Pressure

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RAPID ACTING MECHANISM The three nervous reflexes that act rapidly with in seconds are 1] Baroreceptor feedback mechanism 2] Central nervous ischemic mechanism 3] Chemoreceptor mechanism INTERMEDIATE ACTING MECHANISM The three mechanisms that control BP after several minutes of acute pressure changes are 1]Renin-angiotensin vasoconstrictor mechanism 2]Stress relaxation of vasculature 3]Shift of fluid through the capillary walls LONG TERM MECHANISM Kidneyinvolves renal- body fluid feedback 5/16/12

RAPID ACTING MECHANISM

The three nervous reflexes that act rapidly with in seconds are 1] Baroreceptor feedback mechanism 2] Central nervous ischemic mechanism 3] Chemoreceptor mechanism

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BARORECEPTOR MECHANISM

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BARORECEPTOR FEEDBACK MECHANISM

Baroreceptors are the receptors which respond to stretch. Stretch of vessel wall or chambers of the heart stimulates the baroreceptors. LOCATION 1] Carotid sinus 2] Aortic arch 3] Walls of atria - In right atria around the openng of superior and inferior vena cava. - In left atria around the openings of pulmonary veins

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Carotid sinus

At the bifurcation of the common carotid arteries the root of internal carotid artery shows a little bulge has stretch receptors in the adventitia are sensitive to arterial pressure fluctuations

Aortic arch.
baroreceptors

are also present in the adventitia of the arch of aorta have functional characteristics similar to the carotid sinus receptors. their afferent nerve fibers travel in the aortic nerve, which is a branch of the vagus nerve. (Xth cranial nerve)
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2) Buffer nerves activity

The carotid sinus nerves and vagal fibers from the aortic arch are commonly called the buffer nerves At normal blood pressure levels, the fibers of the buffer nerve discharge at a low rate. When the pressure in the sinus and aortic arch rises, the discharge rate increases; when the pressure falls, the rate declines.

Atrial Baroreceptors
BAINBRIDGE

REFLUX

Rapid infusion of saline or blood into a heart with bradycardia produces reflux tachycardia and hypotension. Increased venous return stimulate atrial baroreceptors leading to tachycardia.

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Ventricular Baroreceptors
When

veratridine is injected into the left coronary artery, the effects produced are reflux apnoea followed by rapid breathing,hypotension and bradycardia. are mainly present in left ventricular wall. reflux is called Bezold-Jarisch reflux.

Receptors

This

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B.P. is regulated neurally through centers in medulla oblongata:

cardiac control centers in medulla oblongata
1. Cardiacaccelerator center (V.M.C)
Sympathetic n. fibers

2. Cardiacinhibitory center (C.I.C)

Parasympathetic n. fibers

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CHEMORECEPTOR MECHANISM

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CHEMORECEPTORS
Peripheral

(ventilation)

Sense low O2 Carotid and aortic (glomus cell) Synapse with IX and X, respectively

Central (medulla/CNS)

Sense low pH primarily

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Reflex involving arterial chemoreceptors Chemoreceptors: situated in the carotid body and aortic body

They have a very rich blood supply, which make them ideal for sampling chemical changes in the blood. Chemoreceptors are sensitive to the decreased Po2, increased PCO2 and increased hydrogen ion concentration in the plasma. Afferent: Afferent nerve fibers form the carotid body travel in the carotid sinus nerve, which is a branch of glossopharyngeal nerve. Aortic body is innervated by the aortic nerve, which is a branch of the vagus
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Response: Stimulation of chemoreceptors leads to a reflex increase in vasomotor tone, which causes generalized vasoconstriction and hence a rise in blood pressure. Importance: Chemoreceptor mechanism is important in regulation of blood pressure when it fall below the range in which baroreceptors act (70 mmHg).

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Net result of Chemoreceptor stimulus is an integration of central and peripheral chemoreceptors

Stretch of pulmonary receptors 5/16/12 cancel peripheral stimulus on cardio-inhibitory area

CNS ISCHEMIC RESPONSE

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(3) CNS ischemic response

Chemoreceptor reflex is useful in regulation of blood pressure when it falls to a level between 40 and 70 mmHg. But if the blood pressure below 40 mmHg, the last ray of hope for survival is the central nervous system (CNS) ischemia response. So it sometimes called the last ditch stand pressure control mechanism.

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As the name indicates, it is evoked by ischemia (poor blood flow) of the central nervous system. CNS ischemia reduces blood flow to the vasomotor centre (VMC). Reduction in blood flow to the VMC leads to reduced Po2 and elevated Pco2 in the medulla region. Both these factors stimulate the VMC directly, leading to vasoconstriction and consequently rise in blood pressure.

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Neurons in the vasomotor center respond directly to the lack of blood flow by maximally stimulating the sympathetic outflow. Believed to be the result of a buildup of CO2. It can increase pressure to 250 mmHg for as long as 10min.This response is stimulated when pressure falls to <60 mmHg and is maximally stimulated at a pressure of 10-15 mmHg
(emergency control system).

Typically slows heart rate somewhat allowing max. 5/16/12 time for oxygen uptake in lung

Cushing Reaction: If cerebro-spinal fluid pressure exceeds arterial pressure, arterial blood flow to the brain stops, this then triggers VMC leading to vasoconstriction and increase in blood pressure until blood flow returns to normal. There is simultaneous stimulation of CIC and the reflux hypertension is associated with bradycardia
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INTERMEDIATE ACTING MECHANISM

The three mechanisms that controll BP after several minutes of acute pressure changes are 1]Renin-angiotensin vasoconstrictor mechanism 2]Stress relaxation of vasculature 3]Shift of fluid through the capillary walls

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RENIN -ANGIOTENSIN MECHANISM

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Angiotensin I

very potent vasoconstrictor formed in the plasma through a chain reaction.

The chain is triggered by a substance, renin, released form kidneys. Renin is released from kidneys in response to renal ischemia, which may be due to a fall in blood pressure.

Effect of Angiotensin II

powerful constrictor release aldosterone from the adrenal cortex acts on the brain to create the sensation of thirst. inhibit the baroreceptor reflex and increase the release of norepinephrine from the sympathetic postganglionic fiber.

STRESS RELAXATION OF VASCULATURE

When the pressure in the blood vessels becomes too high, they become stretched and keep on stretching more and more for minutes or hours; as a result, the pressure in the vessels falls toward normal. This continuing stretch of the vessels, called stressrelaxation, can serve as an intermediate acting mechanism and is termed as pressure buffer.

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SHIFT OF FLUID THROUGH THE CAPILLARY WALLS

When

the capillary pressure falls too low,fluid is absorbed from the tissues into the capillaries of the circulation by osmosis. increases the blood volume and helps to return the blood volume and pressure towards normal. when capillary pressure rises too high,fluid is lost out of circulation,thus reducing blood volume and arterial pressure.
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This

Conversely

LONG TERM MECHANISM

Kidneyinvolves renal -body fluid feedback

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The Renin-Angiotensin System:

Its Role in Pressure Control and Hypertension

Renin is an enzyme which is released by the kidneys when ABP falls too low. Renin is synthesized and stored in an inactive form (prorenin) by the juxtaglomerular cells of the kidney (modified smooth muscle cells located in the wall of the afferent arterioles immediately proximal to the glomeruli). Decreased BP in the afferent arteriole results in release of renin from prorenin.

Renin is an enzyme, not a vasoactive substance!

It acts on another compound in plasma (angiotensinogen) to form angiotensin I (AI). ACE (angiotensin converting enzyme) converts AI to AII.
(Scheme)

Angiotensin II is a powerful vasoconstrictor and increases ABP by increasing TPR increasing venous return to the heart (increasing cardiac output) decreasing excretion of both salt and water (long-term effect)

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Renin Angiontensin Aldosterone in Pressure Regulation

Pa
Renal perfusion pressure

Angiotensinoge n

Renin

Angiotensin I
Angiotensin converting Enzyme, ACE

Angiotensin II

Aldosterone Na+ reabsorption Blood volume

Constriction of arterioles ( TPR)

Pa toward normal

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Renin
Renin is a protease which cleaves angiotensinogen to angiotensin I Renin is secreted by the juxtaglomerular apparatus in response to:

1: reflexive sympathetic activity or beta receptor stimulation 2: decreased central volume of blood 3: decreased plasma Na+ 4: decreased distension of renal arteries

Angiotensin II
One of the most potent vasoconstrictors known Octapeptide (8 amino acids) Constricts principally arteriolar smooth muscle to increase resistance Stimulates the vasomotor center of the brain Stimulates release of Aldosterone (steroid hormone) by the adrenal medulla

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Effect of Angiotensin to Cause Retention of Salt and Water

Direct Renal Effect (can decrease urinary output 4-6 fold)

-Constriction of the renal blood vessels to reduce filtration - Reduction in peritubular capillary pressure, allowing rapid osmotic reabsorption of fluid from the tubules -Increasing tubular reabsorption of water and salt
Stimulation of Aldosterone Secretion from the adrenal glands

- Increase in salt reabsorption by the kidney tubules, increase in extracellular fluid sodium and water retention
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Aldosterone
Steroid

hormone secreted by adrenal medulla in response to angiotensin II formation blood volume by promoting reabsorption of sodium blood volume

Increases

Increases Takes

hours to be effective in raising blood pressure and volume because it requires protein synthesis
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Renin-Angiotensin System: renal blood flow &/or

Na+

++ Juxtaglomerular apparatus of kidneys (considered volume receptors) Renin Angiotensinogen Angiotensin I

Conver ting Angiotensin II enzym (powerful (powerful es vasoconstrictor) vasoconstrictor) Adre nal Corticosterone Aldosterone corte N.B. Aldosterone is the main regulator 5/16/12 x (Lun Angiotensin III gs)

Antidiuretic Hormone (ADH, Vasopressin)

1.

ADH is an oligopeptide released by the posterior pituitary gland into the bloodstream in response to peripheral sensors. ADH release is stimulated by osmoreceptors in the anterior pituitary, triggers ADH and thirst (2% osmolarity change is enough). Angiotensin II also stimulates ADH release by acting on cells in the 3rd and 4th ventricles. Atrial sensors (venous-atrial junctions) sense decreased stretch and send signals via vagal afferents to stimulate the release of ADH
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1.

1.

1.

ADH (Vasopressin) receptors

V1 receptors are in vascular smooth muscle V2 receptors are in the principal cells of the renal collecting duct. These V2 receptors are involved in water reabsorption in the collecting duct and in maintenance of body osmolarity

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ADH (Vasopressin) and Blood Volume

Ang II receptors Osmo receptors Increased osmolarity Optic chiasma

SON PVN

Hypothalamus Maxillary Body

ADH
Anterior Pituitar y

Posterior Pituitary H2 O H2 O H2 O

Vagal afferents

Atrial volume receptors

TPR

Volume Retentio 5/16/12 n

THANK YOU

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