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Blood Flow Control Local & Humoral

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Blood Flow Control Local & Humoral

Uploaded by

Farwa Arshad
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Local and humoral Control of

Blood flow by Tissues

Dr. Saman Saeed

MPhil Physiology, PhD scholar


Chapter:15 Guyton 14th edi
• Each tissue control its own local blood flow in
proportion to its metabolic needs.
Local Control
of Blood
Flow in
Response to
Tissue Needs
Variation in blood flow in different tissues and organs
Mechanisms of Blood Flow Control

1. Acute control
 By rapid changes in local vasodilation or vasoconstriction of the arterioles,
metarterioles, & precapillary sphincters, occurring within seconds to minutes

2. Long term control


 Controlled changes in flow over a period of days, weeks, or even months.

 Due to ↑ and ↓ in the physical sizes and numbers of actual blood vessels
supplying the tissues
Acute Control of Local Blood Flow

 Effect of tissue metabolism on local blood flow . . . ?

 Effect of oxygen availability on local blood flow . . . ?

Vasodilator theory
Oxygen lack theory
Effect of Tissue Metabolic Rate on Tissue Blood Flow
Effect of Tissue Oxygen Conc on Blood Flow
Vasodilator Theory

 There is formation of vasodilator substances in the tissue cells &


act on pre-capillary sphincters, metarterioles, and arterioles.
Whenever
• Greater rate of metabolism

ii. Less availability of O2


iii
. Nutrients to tissue ↓
Vasodilator Theory for Blood Flow Control

TISSUE RELEASE OF
METABOLIS VASODILATOR
M S

ARTERIOLE
Adenosine adenosine CO2 RESISTANC
phosphate E

BLOOD
histamine K+ & FLOW
H+
ions
Oxygen Demand Theory for Blood Flow Control

TISSUE OXYGEN
OXYGEN DELIVERY CONCENTRATION
TO TISSUES

ARTERIOLE
RESISTANC
E

BLOOD
FLOW
 Examples of Acute "Metabolic" Control of Local Blood Flow

1. Reactive Hyperemia
 As a reaction to the blockage of the blood supply

• Active Hyperemia
 Whenever tissue becomes active
1. Exercising muscle
Autoregulation of Blood Flow
when B.P. changes

 In any tissue of the body, acute ↑ in B.P. causes B.F. to ↑


but B.F. returns back to normal.

 B/w B.P. 70-175 mmHg blood flow remains autoregulated.

 Two basic mechanisms


• Metabolic theory

• Myogenic theory
Metabolic Theory

Increase in B.P. provides more O2 and nutrients to the


tissue.

Excess O2 causes blood vessels to constrict and the flow


returns back to normal despite increased pressure.
Myogenic theory

 When B.P. ↑ there is ↑ stretch of vessels wall causes the smooth muscle of
vessels wall to constrict that reduces blood flow nearly back to normal.

 When B.P. ↓ the degree of stretch of the vessel is less → smooth muscle
relaxes → reducing vascular resistance and helping to return flow
toward normal.
Long-term Regulation of Blood Flow
 More effective than acute mechanism.

 Long-term local blood flow regulation occurs by changing the degree of


vascularity of tissues (size and number of vessels).

 Oxygen is an important stimulus for regulating tissue vascularity.


Long-Term Blood Flow Regulation
 New B.V. are formed within a few weeks to match the needs of the
tissue.

 Important angiogenic factors:


• Vascular endothelial growth factor

• Fibroblast growth factor

• Angiogenin

 Development of collateral circulation is basic phenomenon


Humoral Control of the Circulation
By substances secreted or absorbed into body fluids e.g. hormones & ions.

Vasoconstrictor Agents Vasodilator Agents


i. Norepinephrine and i.Bradykinin
Epinephrine
ii.Histamine
ii. Angiotensin II
iii.Serotonin
iii Vasopressin
iv.Prostaglandins
.
iv. Endothelin
v.Nitric oxide
Norepinephrine and Epinephrine
 Norepinephrine is more powerful vasoconstrictor than
epinephrine.

 During sympathetic stimulation e.g. in stress or exercise, nor epi


& epi are released at nerve endings.

 Effect is ↑ excitability of heart and vasoconstriction of arterioles


& veins
Norepinephrine and Epinephrine

 Sympathetic N.S. stimulation also stimulates adrenal medulla


which secrete both norepinephrine & epinephrine .

 These hormones then circulate to all areas of the body and cause almost the
same effects on the circulation as direct sympathetic stimulation, thus
providing a dual system of control.
2. Angiotensin II
 Powerful vasoconstrictor

 Main effect is on arterioles

 Total peripheral resistance increases → B.P. ↑

• Endothelin
 A powerful vasoconstrictor having 21 amino acids

 Endothelin present in endothelial cells of all blood vessels.

 Released when there is damage or crushing injury to blood vessels


4. Vasopressin (Antidiuretic hormone)
 more powerful than angiotensin II

 formed in the hypothalamus, transported and stored in the


posterior pituitary gland

 Reabsorption of water from the renal tubules back into blood to control body
water.

 Volume of urine is decreases hence called Antidiuretic hormone


Bradykinin

 Bradykinin causes arteriolar


dilation and increases capillary
permeability

 Bradykinin also helps to regulate


blood flow in the skin, in salivary
and GI glands
Histamine
 Histamine is released in almost every tissue of the body if the tissue
becomes damaged or inflamed or is the subject of an allergic reaction.

 Derived from mast cells in the damaged tissues and basophils in the blood

 Cause arteriolar dilation and increase capillary permeability leaking of


fluid edema
Vascular Control by Ions and Other Chemical Factors

 ↑ in Ca++ conc → vasoconstriction

 ↑ in K+ ion → vasodilation

 ↑ in Mg++ ion → powerful vasodilation


 Both potassium and magnesium ions inhibit smooth muscle
contraction
Vascular Control by Ions and Other Chemical Factors

 ↑ in H+ (acidosis or ↓ in pH) → dilation of the arterioles.

 ↓ in H+ (alkalosis or ↑ in pH) → arteriolar constriction.

 Anions (acetate and citrate) cause mild degrees of


vasodilation.
Vascular Control by Ions and Other Chemical Factors

 An increase in CO2 conc → causes moderate vasodilation in most

tissues but marked vasodilation in the brain.

 CO2 in the blood also has an extremely powerful indirect effect on

vasomotor center → sympathetic stimulation → vasoconstriction

throughout the body


Reference:

Guyton & Hall Chap: 17, 14th Edi

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