>>Dr. Ketchum: In this video lecture, we are
going to be focusing on the regulation of mean arterial pressure, specifically the long-term
regulation. So just to quickly recap, long-term regulation takes minutes to days to go into
effect. It involves the kidneys, which then the kidneys can regulate your blood volume.
By regulating blood volume, you can regulate the mean arterial pressure. So let’s see
how this is done. On this diagram, what we’re going to be
studying is the renin-angiotensin system and how the renin-angiotensin system controls
arterial pressure. Remember that this is a long-term regulation. And we are going to
be beginning with a, a situation where you have a decreased MAP. So MAP is low. Now there’s
several different pathways occurring in this diagram, and so be real careful as we go through
this what—what specific pathway we’re talking about. So I’m going to take you
through the shortest pathway first. So when the mean arterial pressure is lowered, that
gets detected by the kidneys. And when the kidneys detect this low mean arterial pressure,
they produce less filtrate. So what this means is that you urinate less. So if we urinate
less, then that’s going to increase the blood volume and by increasing the blood volume,
that will increase MAP, because remember, that needs to be the goal. If we start with
a low MAP, the goal needs to be to return MAP back to normal by elevating it to the
normal level. Now that’s just one pathway. Now let’s go ahead and follow another pathway
here. So while that is happening, you also have baroreceptors that are detecting the
low MAP. And so my question for you is when MAP is low, what exactly are the baroreceptors
detecting and what is their response? So would there be a lot of stretch detected by the
baroreceptors or a little stretch detected by the baroreceptors? The correct answer is
that there would be little stretch compared to normal…that gets detected by the baroreceptors.
Because there’s less stretch detected by the baroreceptors, they’re going to send
a low frequency of action potentials, right? They’re going to develop a low frequency
of action potentials, which is going to wind up causing a sympathetic response. So once
we have this sympathetic response, what happens now is the sympathetic response will target
the kidneys. The kidneys, then, will synthesize and secrete renin. Renin is an enzyme. This enzyme then catalyzes
a whole bunch of reactions that we’ll talk more about later. In fact, this is in the
urinary system. And so ultimately, what happens through these series of enzyme catalyzed reactions
is the formation of a hormone called angiotensin II. So this hormone then, angiotensin II targets
the adrenal cortex, specifically the zona glomerulosa. And when it targets the glomerulosa,
that’s going to cause a synthesis and secretion of aldosterone. So remember what the function
of aldosterone—it increases the sodium reabsorption. So if we reabsorb sodium, water follows, so
that’s going to increase water reabsorption by the kidneys as well. By increasing sodium
reabsorption and therefore increasing water reabsorption, the blood volume goes up, which
then increases the arterial pressure. Okay, now angiotensin II will also target
the posterior pituitary. And when it targets the posterior pituitary, that’s going to
cause the release of ADH—antidiuretic hormone. Remember that antidiuretic hormone is also
called vasopressin. So antidiuretic—it’s not a diuretic. It does the opposite, so you’re
going to urinate less. We urinate less, and the reason we’re urinating less is because
of increased water reabsorption. Therefore, once again, if you increase water reabsorption,
your blood volume goes up and your MAP will go up as well. Now there’s also a couple of intrinsic controls
here as well. And so I’m going to put these intrinsic controls in blue for you, because
angiotensin II also causes vasoconstriction— this is an intrinsic control—of the blood vessels.
So if they vasoconstrict, that’s going to increase resistance, and when we increase
resistance, the arterial pressure goes up as well. Now what’s not shown on this diagram
is that ADH can also be intrinsically controlled and that can cause vasoconstriction as well.
So both angiotensin II and ADH can both cause vasoconstriction, which increase resistance
and increase MAP. So this is the long-term mechanism using the kidneys to regulate your
mean arterial pressure. So let’s take an example. How does all of this work? Let’s
put it all together. So what I would like for you to do is pause the video and then
I would like you to use up or down arrows to indicate whether or not you think the level
for each of these would go up or go down based on a patient that is hemorrhaged. So if you
had a patient that hemorrhaged this means that they lose a lot of blood, huge amounts
of blood. So pause the video, fill this out, and when you’re ready, replay the video to
see if your responses are correct. Okay, so I’m going to assume that you’ve
already paused the video and you’ve already put your answers in so let’s—let’s go
through this. If you hemorrhage, your blood volume is going to go down. You’ve lost
a large component of your blood volume, which can cause—if there’s less blood volume,
your central venous pressure is going to go down. When that pressure goes down, there’s
less venous return, which is going to cause your end-diastolic volume to go down, which
causes your cardiac output to go down as well. Now if cardiac output goes down, how do you
think this will affect your end-systolic volume? Well, if you’re ejecting less blood, your
end systolic volume should be high. All right, so if cardiac output goes down we know based
off of the formula then that MAP is also going to go down, and so now the kidneys need to
respond. So the kidneys respond by producing less urine, right? So we’re going to be
conserving water, conserving salts, which will then increase your blood volume. If you
increase your blood volume that will increase your central venous pressure, if there’s
higher pressure that means you get more blood returning to the heart, so the venous return
goes up. The more blood that comes into the heart the larger end-diastolic volume, okay,
which causes your cardiac output to go up. If cardiac output goes up, your stroke volume
is going to go down, right? The larger ejection means there’s less left in the heart. So
ESV would go down, and finally, if cardiac output goes up, MAP is returned to normal.
So remember that MAP fell drastically because you hemorrhaged, and now that MAP is elevated
and so the system will shut off via negative feedback. Now you can also come over this direction
of your flow chart and I would suggest adding the sympathetic response as well that—that
you would have according to the image prior to this one. So here are a summary of the
factors that actually increase MAP—and this is a nice little summary for you. It also
includes your chemoreceptors, remember, we talked about those with reference to respiration.
And so this is not an all-inclusive summary; it just gives you an idea. It’s a good way
for you to start putting together all the factors that increase MAP, but there certainly
are some things you could add to this to make it more complete. This will conclude the video
on long-term regulation of mean arterial pressure.

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5 thoughts on “Human Physiology – Long Term Regulation of Mean Arterial Pressure”

  1. Amazing video! Only error is at the end when you say ESV goes down you said "End Stroke Volume" goes down instead of "End Systolic Volume"

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