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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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