Regulation of Arterial B.

P:
1) 2)

SHORT TERM REGULATION LONG TERM REGULATION

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

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 functional when M.B.Pr changes b/w 60180 or upto 210 mmHg. (within limits).

When Mean B.P falls below 60 or rises beyond 180 mmHg, there is no additional stimulation of Baroreceptors, so these are maximally stimulated in this range. Why Baroreceptors are not suitable for Long Term Regulation???

Baroreceptors undergo ADAPTATION in 24-48 hrs. So if a change in B.P persists for more than 48 hrs, the Baroreceptors dont remain effective as in Hypertensive patients. So they are reset at a higher pressure.

When B.P increases more stretch of Baroreceptors more impulses go to V.M.CSYMPATHETIC INHIBITION & PARASYMPATHETIC STIMULATION C.O, Peripheral Resistance & B.P falls back to normal.

When B.P decreases less stretch of Baroreceptors less impulses go to V.M.C.SYMPATHETIC STIMULATION & PARASYMPATHETIC INHIBITION Tachycardia & peripheral V.C. B.P back to normal.

Baroreceptors maintain B.P during postural changes. 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 from Baroreceptors are called: PRESSURE BUFFER NERVES (Hering N which is a branch of Glossopharyngeal N & Sensory N fibers of Vagi)

Baroreceptor reflexthe response to B.P:

B.P Firing of Baroreceptors in carotid artery & aorta sensory neurons stimulate V.M.C (Cardiovascular control centre in medulla) sympathetic part & parasympathetic part.

HIGH B.P BARORECEPTORS + V.M.C Less SYMP Negative feed back

PARASYM More A.Ch at muscarinic receptor Beta1 receptor Vent.myocar Less force of contr Less C.O

Less Nor-Adr released Alpha receptor ArterioS.M V.D Less TPR

SA Node
Less H.Rate

LOW B.P

When increase in Mean B.P<60 mmHg & I.Cr.Pr>45mmHg (within limits) CNS Ischemic response + VMC Ischemia more symp. Discharge(V.C nerves) Tachycardia + Periph V.C Increased B.P (Last attempt of body to save life).

2) CHEMORECEPTORS: (Role in Short Term Reg.)

Help to increase B.P when Mean B.P becomes very low (<60mmHg). M.B.Pr<60sluggish B.Flow more pCO2, less pO2 & less pH stimul. Of Chemoceptors in carotid & aortic bodiesimpulses to VMCSymp. Stimulation: ( tachycardia + peripheral V.C) B.P

3) Veno-constriction:
When B.P decreases symp.Stimulation veins constricted Mean systemic filling pr (MSFP) increases Venous return increases C.O & B.P.

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.

HORMONAL MECHANISMS(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. stimulation H.Rate & periph. V.C.

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.

CONSTANTLY PRODUCES
LIVER

ANGIOTENSINOGEN IN PLASMA

J.G CELLS OF KIDNEY

B.P PRODUCE RENIN

ENDOTHELIAL CELLS OF LUNG CAPILLARIES

ANGIOTENSIN 1
DECAPEPTIDE IN PLASMA

CONTAIN ANGIOTENSIN-CONVERTING ENZYME (A.C.E) ANGIOTENSIN 2 OCTAPEPTIDE IN PLASMA CIRCULATES IN BLOOD FOR FEW MIN.

THEN DESTROYED BY ANGIOTENSINASE IN R.B.Cs etc

ROLE OF ANG2 IN SHORT+LONG TERM CONTROL OF B.P:(in 20 min)

ANG2
(Short-term) (LONG TERM )

Arterioles

VMC

Hypothalamus

Adrenal cortex
ALDOSTERONE

(cvs response) V.C Important in short term regulation only

ADH

THIRST

Na reabs

(VOL & OSMOLARITY)

B.P

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

MISCELLANEOUS MECHANISMS OF SHORT TERM REGULATION OF B.P:

1) CAPILLARY FLUID SHIFT: 2) STRESS RELAXATION: 3) REVERSE STRESS RELAXATION:

5/24/2007

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

When B.P Cap. pr fluid passes from blood I.S. Spaces B. Vol V.R B.P

STRESS RELAXATION:

When changes in B.P are due to changes in B. Volume, there are compensatory changes in size of B. 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)

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 is property of smooth muscle. Smooth muscle can change its size without change in pr. Smooth muscle in stomach wall also relaxes to allow extra food volume without in pr. Also urinary bladder & uterine smooth muscle show this property to accommodate volume.

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 the vascular system. SIGNIFICANCE: It prevents development of hypovolemic shock.

IMPORTANT:

One factor for shock development is disparity b/w blood 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 relaxation cant prevent shock because of loss of Vasomotor tone disparity b/w blood vol. & capacity of vascular system.

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.

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.

When B.P Renal blood flow Glomerular pr GFR Salt & water lost in urine blood vol V.Return C.O B.P to normal. When B.P changes, there are marked changes in urinary output. Suppose B.P to 200mmHg urine output If B.P below 60mmHg Anuria

Changes in blood vol marked 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.

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 is V.C in tissues (because tissues at rest do not require 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.

Significance of giving diuretics to hypertensives:

We decrease blood volume to decrease B.P, CAUSE THERE IS 3555% INCREASE IN B.P WITH ONLY 2% INCREASE IN BLOOD VOLUME.

4 FACTORS ASSISTING RENAL BODY FLUID Pr CONTROL MECHANISM:

1) 2) 3) 4)

SYMP. IMPULSES TO KIDNEY. RENIN ANGIOTENSIN MECH. ADH MECHANISM. ALDOSTERONE.

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.

Suppose B.P ?

SYMP. Impulses to kidney RENIN ADH ALDOSTERONE Net effect: Retention of salt & water.

% COMPENSATION BY SHORT Vs LONG TERM REG:

Compensation of B.P by SHORT TERM REGULATION is 85-90% Compensation of B.P by LONG TERM REGULATION is 100% but takes many hrs to few days to become activated.

100% 85-90%

R.B. Fl pr control

CNS Ischemic response

Max. feedback gain at opt .pr

Baroreceptors Chemoreceptors

Stress relaxation Cap. Fl shift Sec. Min. Hrs. days TIME