Circulation, Regulation of Blood Pressure

7/28/2019 Circulation, Regulation of Blood Pressure

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Regulation of Arterial

B.P:

1) SHORT TERM REGULATION

2) LONG TERM REGULATION


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SHORT TERM

REGULATION: It maintains B.P when there are rapid

changes in B.P:

-Postural changes-Sudden loss of blood from the body.

3 types of mechanisms:

-Nervous-Hormonal

-Miscellaneous


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Nervous Mechanism of Short

Term Regulation of B.P:Very rapid. Activated in seconds.

A) BARO-RECEPTOR REFLEX

MECHANISM:-

Stimulation Range (autoregulation):

These receptors remain functionalwhen M.B.Pr changes b/w 60180 orupto 210 mmHg. (within limits).


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When Mean B.P falls below 60 or risesbeyond 180 mmHg, there is no

additional stimulation ofBaroreceptors, so these are maximallystimulated in this range.

Why Baroreceptors are not suitable forLong Term Regulation???


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Baroreceptors undergo ADAPTATIONin 24-48 hrs.

So if a change in B.P persists for morethan 48 hrs, the Baroreceptors dontremain effective as in Hypertensive

patients. So they are reset at a higherpressure.


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When B.P increases more stretch ofBaroreceptors more impulses go to

V.M.CSYMPATHETIC INHIBITION &PARASYMPATHETIC STIMULATION

C.O, Peripheral Resistance & B.P

falls back to normal.


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When B.P decreases less stretch ofBaroreceptors less impulses go to

V.M.C.SYMPATHETIC STIMULATION& PARASYMPATHETIC INHIBITION

Tachycardia & peripheral V.C.

B.P back to normal.


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Baroreceptors maintain B.P during posturalchanges.

They minimize diurnal variation in B.P.

( A.M, P.M by 5-10 mmHg)

Baroreceptor mechanism=pressure buffer system.

Sensory nerves which carry impulses fromBaroreceptors are called:

PRESSURE BUFFER NERVES (Hering N which is abranch of Glossopharyngeal N & Sensory N fibers ofVagi)


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Baroreceptor reflex-

the response to

B.P: B.P Firing of Baroreceptors in

carotid artery & aorta sensory

neurons stimulate V.M.C(Cardiovascular control centre inmedulla) sympathetic part &

parasympathetic part.


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PARASYM

Less Nor-Adr released More A.Ch at muscarinic receptor

Alpha receptor Beta1 receptor

SA NodeVent.myocarArterioS.M

V.D Less force of contr Less H.Rate

Less TPRLess C.O

LOW B.P

Less SYMP

V.M.C

BARORECEPTORS

HIGH B.P

Negative feed back

+


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When increase in Mean B.P45mmHg (within limits)

CNS Ischemic response + VMCIschemia

more symp. Discharge(V.C nerves)

Tachycardia + Periph V.CIncreased B.P (Last attempt of body tosave life).


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2) CHEMORECEPTORS:

(Role in Short Term Reg.) Help to increase B.P when Mean B.P

becomes very low (


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3) Veno-constriction:

When B.P decreases

symp.Stimulation veins constricted

Mean systemic filling pr (MSFP)increases

Venous return increases C.O & B.P.


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4) Increased contraction

of SKELTAL MUSCLES: When B.P falls symp. Stimulation

Increased force of skeletal muscle contraction(including abdominal &

thoracic muscles) V.Return C.O & B.P.

THESE ARE THE NERVOUS MECHANISMS

ACTIVATED IN SECONDS IN SHORT TERM

REGULATION OF B.P.


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HORMONALMECHANISMS(short+long

term regulation of Art. B.P) 1) CATS(CATECHOLAMINES):

When B.P SYMP stimulation

release of CATS from Adrenal Medulla

same CVS effects as of direct symp.

stimulationH.Rate & periph. V.C.


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2) RENIN-ANGIOTENSIN MECHANISM:

When B.P to low value

Renal B.Flow Glomerular Pr

(normal glomerular pr=60mmHg)

GFR Less conc. Of Na & Cl

at macula densa (a part of J.G

apparatus) is sensed Renin release

from J.G cells. Also released in response

to Symp. Stimulation. Renin persists in blood for

one hour.


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LIVER

CONSTANTLY PRODUCESANGIOTENSINOGEN

IN PLASMA

B.P

J.G CELLS OF KIDNEY

PRODUCE

RENIN

ANGIOTENSIN 1

DECAPEPTIDE IN PLASMA

ANGIOTENSIN 2

OCTAPEPTIDE IN PLASMA

ENDOTHELIAL CELLS OF LUNG CAPILLARIES

CONTAIN ANGIOTENSIN-CONVERTING ENZYME (A.C.E)

CIRCULATES IN BLOOD FOR FEW MIN.

THEN DESTROYED BY ANGIOTENSINASE IN R.B.Cs etc


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ROLE OF ANG2 INSHORT+LONG TERM

CONTROL OF B.P:(in 20 min)

Arterioles

ANG2

VMC Hypothalamus Adrenal cortex

(Short-term) (LONG TERM )

V.C

Important in short term regulation only

(cvs response) ADH THIRST

(VOL & OSMOLARITY)

ALDOSTERONE

Na reabs

B.P


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3) VASO-PRESSIN/ADH Mechanism:

When B.P Release of ADH

from hypothalamo-neuro-hypophyseal system.

ADH (synth. in hypoth) (transported to) Post.pituitary

ADH release

ADH has 2 actions:

1) V.C/VASOPRESSIN IN SHORT-TERM REGULATION

2) ANTIDIURETIC HORMONE REABSORBS WATER FROM D.C.T FOR LONG-TERM


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MISCELLANEOUSMECHANISMS OF SHORT

TERM REGULATION OF B.P: 1) CAPILLARY FLUID SHIFT:

2) STRESS RELAXATION:

3) REVERSE STRESS RELAXATION:

5/24/2007


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CAPILLARY FLUID SHIFT:

When B.P Capillary pr

movement of fluid from blood to

I.S.Spaces blood volume V.R

B.P

B.P Cap .Pr


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When B.P Cap. pr fluid

passes from blood I.S. Spaces

B. Vol V.R B.P


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STRESS RELAXATION:

When changes in B.P are due tochanges in B. Volume, there are

compensatory changes in size ofB. Vessels, so that B.P is regulated.

e.g, on massive blood transfusion

B.P Then within 1 hr

NORMAL B.P (due to stress relaxation)


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Mechanism of Stress

relaxation: Smooth muscle in vessel wall undergoes relaxation,

so that even

B. Vol can be accommodated & B.P

falls back. This property of stress relaxation isproperty of smooth muscle. Smooth muscle canchange its size without change in pr. Smoothmuscle in stomach wall also relaxes to allow extrafood volume without

in pr. Also urinary bladder & uterine smoothmuscle show this property to

accommodate volume.


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REVERSE STRESS

RELAXATION: When B.P falls due to blood loss,

smooth muscle in vessel wall contracts

around blood volume, so that even blood vol. can adequately fill thevascular system.

SIGNIFICANCE:

It prevents development ofhypovolemic shock.


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IMPORTANT:

One factor for shock development is disparity b/wblood vol. & capacity of vascular system.

In Neurogenic shock, blood vol is same but because

of loss of vasomotor tone disparity shock.

In neurogenic shock reverse stress relaxationcant prevent shock because of loss of Vasomotor

tone

disparity b/w blood vol. & capacity ofvascular system.


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LONG TERM REGULATION

OF B.P: This maintains B.P for days, weeks,

months or even years.

It involves Renal Body Fluid Pr Control

Mechanism.This is called Pr. Diuresis

& Natriuresis.


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NATRIURESIS/Pr.

DIURESIS: When B.P Renal blood flow

Glomerular pr GFR

salt & water excretion in urine

blood volume V.Return

C.O B.P falls back to normal.


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When B.P Renal blood flowGlomerular pr GFR Salt& water lost in urine blood volV.ReturnC.O B.P to normal.

When B.P changes, there are markedchanges in urinary output.Suppose B.P to 200mmHg urine outputIf B.P below 60mmHg Anuria


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Changes in blood volmarked effect on B.P: Suppose in a person there is 2%

persistent in B.Vol, this 2%

V.Return 5% in C.O

Regarding blood flow to tissues,

there is a LOCAL CONTROL

MECHANISM.


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LOCAL BLOOD FLOW

CONTROL MECHANISM: Normally tissues are supplied by minimum amount

of blood. When 2% in B.Vol & 5% in C.O

there is autoregulation in tissues. Normally there isV.C in tissues (because tissues at rest do notrequire amount of blood) TPR.

So due to C.O,TPR also due to autoregulatory V.C in tissues

B.P (due to both in C.O & in TPR).So there will be 35-55% in B.P with only 2%in blood vol.


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Significance of givingdiuretics to hypertensives:

We decrease blood volume todecrease B.P, CAUSE THERE IS 35-

55% INCREASE IN B.P WITH ONLY2% INCREASE IN BLOOD VOLUME.

4 FACTORS ASSISTING


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4 FACTORS ASSISTINGRENAL BODY FLUID Pr

CONTROL MECHANISM: 1) SYMP. IMPULSES TO KIDNEY.

2) RENIN ANGIOTENSIN MECH.

3) ADH MECHANISM.

4) ALDOSTERONE.


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Suppose B.P ? SYMP impulses to kidney are inhibited

V.D in kidney salt & water loss.

RENIN-ANGIOTENSIN will not be activated. ADH & ALDOSTERONE are not activated.

Net effect: amount of salt & water

loss in urine.


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Suppose B.P ? SYMP. Impulses to kidney

RENIN

ADH

ALDOSTERONE

Net effect: Retention of salt & water.


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% COMPENSATION BYSHORT Vs LONG TERM REG:

Compensation of B.P by SHORT TERMREGULATION is 85-90%

Compensation of B.P by LONG TERMREGULATION is 100% but takes

many hrs to few days to become

activated.


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85-90%

100%

Max. feedback gain at opt .pr

Sec. Min. Hrs. days

R.B. Fl pr control

CNS Ischemic response

Chemoreceptors

Baroreceptors

Stress relaxation

Cap. Fl shift

TIME

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Circulation, Regulation of Blood Pressure