Arterioles side of the location can be thought of a as a reservioir, and the vol of it is
affected by (i)cardia input (ii)cardic output.
Arterioles are gateway to the rest of the circulation. This flow outwards is going to determine
the vol that remains within arteries, and as a result of that vol we are going to have certain
pressure. The pressure witin the arteriole system is determind by the filling volume. So
arterioles do have an impact on the MAP.
Two different sceiniors (arteriole are creating high resistance pathway, very constricted, highly
limited with what can leave arteries) High resistance is called by the sympathetic nervous
system which releases norepinephrine binding to alpha adregneric receptors on the
smooth muscle which will cause arterioles to constrict. (i) of consequence of high resistance
pathway, and impeded blood flow from getting out WE WILL INCREASE MAP.
(ii) Due to high resistance capillaries will have less blood flow that is going to have two different
impacts which will (i) minimize the amount of less gas/nutrient exchange since there is not
enough blood moving through them allowing diffusion to occur (IMPACT ON TISSUE
(ii) When arterioles valves are shut off which limits the blood to enter, we are reducing capillary
pressure (since not enough blood is filling them anymore) . We are reducing the hydrostatic
pressure, but our osmotic protein pressure is the same. We will have greater fluid
reabsorption from the interstitim into the capillaries compared to the filteration process. Those
are two effects on the capillaries and are independent effect. (IMPACT ON BLOOD VOLUME
& INERSITAIL FLUID VOL)
When the arterioles become low resitance, they vasodilate, allowing large radius tubes , which
lowers resistance and allowing more blood to go. When do we have low resistance pathway?
Generally occurs whe we have accumulation of metabolites. Metabolites are major form of
vasodilating.When they accumulate they intitate a signal which is greater than sympathetic
That allows vasodilation to occur and more blood to exist the arteries and go to arterioles.
Cardiac out to be steady its not changing. The MAP when we open up the values , more blood
is existing but same amount is coming in, vol is going to reduced that stays in the arteries. MAP
wil be lower than before.
The more arterioles that vasodilate, the more effect there will be on MAP. A lot of blood will go
and move up to capillaries. Capillaries are now experiencing higher flow. The blood is going to be O2 rich and nutrient rich and remove CO2 and metabolies. We weill get enchaned exchange.
The filling pressure of the capillaries is higher (more blood fills up capillaries. The hydrostatic
pressure is higher , and its going to affect the fluid exchange . When we have more pressure in
the capillaries because arterioles have jus let more blood enter them. There is going to be
higher filteration than absorption( more water will be pushed into surrounding interstitium). The
water will be accumulating and tissue will be swelling up =adema (CHECK SPALLING)
Or the lymph vessels will take that fluid and move it back through the lymph system SO IT
RETRUNS BACK TO THE CIRCULATION
Systolic pressure isincreasing because of Valsalava Manoeuvre (forced expiration against
closed glottis, increasing thoracic pressure will also increase MAP)
Active & Reactive hypermia= both things cause vasodilation; both negative feed backs
designed to restore the metabolic profile of the tissue.
Active Reactive Hypermia
-there is an accumulation of Hyperemia in a part resulting from the
metabolites(adenosine, Co2) locally within the restoration of its temporarily blocked blood
tissue , those metabolites since they cause the flow.
smooth muyscle to relax which cause (e.g cuffs during blood pressure)
vasodilation to occur.
What has caused the accumulation is the
difference between the two.
Tissue has enhanced its metabolic Reactive hypermia, is happening in absence of
activity; more consumption of O2 and change of metabolic activity. So in a muscle that
greater production of metabolites. Active occurs when you have strong contraction , it can
becase the cells are actively consuming happen in skeletal muscle, it temp blocks blood
more oxygen and nutrients from entering that region because the blood
vessels have been compressed by the muscle.
Cells are still metabolizing , the cells are
accumulating because they are not being
*When you restore blood flow then you see
both things cause vasodilation; both negative feed backs designed to restore the metabolic
profile of the tissue. The increase in blood flow will help to washaway metabolites and bring O2 back to
that region blocked due to accumulation of metabolites.
Arterioles VASODILATION does not affect the venous return because the veins lie in between
the two (arterioles and the heart) . The veins determine VENOUS RETURN.
Sympathatic Nervous effect on arterioles and how it fits in with exercise.
Sympathetic nerves release norepinephrine which will cause vasoconstriction, when symp
nervous activates adrenal glands they release epinephrine and in the skeletal muscles that will
allow , for epinephrine to bind to beta adgregneric receptor which will cause some vasodilation.
Balancing amount of norepinephrine vs. epinephrine because of that sympathetic nervous
system to vasoconstricte skeletal muscle blood vessel. When sympathetic is active both are
being released and two have a conflict with each other
Locally produced metabolites are added , that’s the additional point that tips the balance
between vasoconstriction and vasodilation. So when you are excercising we have
norepihinepihne and ephonrine balance. Metabolites will add to the vasodilation part and you
will see vasodilation in the excercising muscle.
In non-exercising is muscle, when sympathetic nerve activity is high in the body, you will see
vasoconstriction in other muscles not EXCERCISING . There we just have norepinephrine
due to more receptors as compared to epinephrine which causes VASOCONSTRICTION.
Net total is vasoconstriction that no