So, glomerular filtration rate and renal blood flow inherently have a link to them. They are
not the same parameter though. What you can think about is that glomerular filtration rate
is going to be fairly constant across most renal blood flows. The renal blood flow is only
constant across an autoregulatory range. If you have too high of pressures or too low of
pressures, you're not going to have the same amount of renal tubule blood flow. If pressure
is high above the autoregulatory range, you're going to have an increase in renal blood flow.
If pressure is below the autoregulatory range, you're going to have a decrease in renal blood
flow. Now what causes this autoregulatory range to have a fairly consistent blood flow across
a wide range of mean arterial pressures? That can be seen in this graft that you see where
you have mean arterial pressure on the X axis or blood flow on the Y axis. There is a range at
which there is autoregulation and that means that through this zone you're going to have a
fairly constant flow despite the changes in mean arterial blood pressure. What causes that?
It's primarily due to a myogenic response. And what is a myogenic response? That is an
inherent local reflex. "If you have too much pressure inside a vessel, it may cause it to
constrict. If there's not enough pressure inside the vessel, it will cause it to dilate on its own."
So those 2 local effects allow for you to maintain renal blood flow across a fairly long mean
arterial pressure zone. Glomerular tubular feedback is also a very important aspect when
trying to determine what renal blood flow is. It doesn't fit quite as well on this particular
graft so we're going to use renal tubule feedback in more of a diagram form. So as we look
for glomerular tubular feedback, let's talk through the 2 different examples that we have.
One is an increase in tubule flow. The second will be a decrease in tubule flow. So what affects
tubule flow and how do you get that to change renal blood flow? The first thing to think
about is what is renal tubule flow being sensed? Well at this point, you can't really stick a flow
meter in your kidney and determine how fast the fluid is traveling through it. So, what the
body does instead is sent the amount of sodium chloride in bulk form that's transported
across the renal tubule. If there is high amount of sodium and chloride that is traveling past
the macula densa, which is in the distal convoluted tubule right next to the juxtaglomerular
cells. There is a little signal that is sensed that decreases the amount of renin release.
If you have a decrease in the amount of renin release, the net result is no angiotensin II
and no aldosterone formed. There is a signal of adenosine that is released in response to
having a high sodium chloride sensed by the macula densa. What that increase in adenosine
does is cause the afferent arteriole to constrict and the efferent arteriole to dilate and the
net result is a decrease in the pressure of the ultrafiltrate, a decrease in glomerular filtration
rate, and that causes tubule flow to decrease. The other example is if tubule flow decreases
too much, how do you get to regulate that through glomerular tubular feedback? And you're
going to do the same thing, you're going to sense the bulk flow of sodium chloride by the
macula densa. This case though, if you have low sodium chloride you're going to get a block
of adenosine. You will, however, increase more renin and as you increase more renin from
these juxtaglomerular cells what this does is increases angiotensin I, angiotensin II.
Angiotensin II in this case is an active substance and angiotensin II causes the efferent
arteriole to constrict. So remember if you constrict the efferent arteriole, you're going to get
a back-up of pressure in the glomerular capillary. This increases the pressure of ultrafiltration.
It increases the glomerular filtration rate. If you increase glomerular filtration rate, then that
result is tubular flow will increase. So looking at glomerular tubular feedback also gives us
insight into how it might change glomerular filtration rate and then even renal blood flow.
Now if we return to this kind of diagram of trying to look at glomerular filtration rate, they're
on the bottom and then renal blood flow with its autoregulatory zone. What other molecules
affect renal blood flow? Nitric oxide and prostaglandin especially prostaglandin E2 cause
dilation of blood vessels and therefore more renal blood flow. The endotheliums and
leukotrienes cause a constriction. Both the nitric oxide and prostaglandins will cause
vasodilation of the various arterioles. To look at this in more detail, let's take our example of
our nephron here. This is the afferent and efferent arterioles. So let's review dilation of first
the afferent arteriole. If you vasodilate this arteriole, you get an increase in ultrafiltration
perfusion pressure, increases in the partial pressure within the glomerular capillary, this
increases GFR and increases tubular flow. The downside of this part here is there's also an
increase in renal blood flow associated with the afferent arteriole. If you remember, if you
dilate the efferent arteriole the opposite effects happen where you have decreases in GFR
and decreases in flow, but this also increases renal blood flow. If we combine these effects
dilating both the afferent arteriole and the efferent arteriole will look something like this. Now
what happens to the overall glomerular filtration rate? It really doesn't change very much if
it's only stimulated a little bit. If you get a little bit of vasodilation of the afferent and
efferent, these can balance each other out and therefore there is no change in glomerular
filtration rate but there is a large increase in renal blood flow. In terms of the endocrine
substances, we've already talked about angiotensin II. We talked about angiotensin II with
the glomerular tubular feedback. If you have an increase in ang II, you get a decrease in
renal blood flow; atrial natriuretic peptide or ANP causes an increase in renal blood flow;
epinephrine, which is also you can think of that as a sympathetic nervous system response of
release from the adrenal medulla that causes a vasoconstriction which would decrease renal
blood flow. And finally we have neuro factors and these neuro factors primarily utilize
norepinephrine as the neurotransmitter of choice and those also have a decrease on renal
blood flow. Now when you get multiple constrictors that can affect both the afferent and
efferent arterioles, we need to combine the effects on glomerular filtration rate and renal
blood flow. So let's review again an afferent arteriole. Vasoconstriction here decreases the
partial pressure of the ultrafiltrate, decreases the pressure of the glomerular capillary
hydrostatic fluid, decreasing GFR, and decreasing the renal tubule flow. This will also decrease
renal blood flow. If we look at the time where you get an efferent arteriole vasoconstriction,
the opposite effects happen on glomerular filtration rate and the ultrafiltration pressures.
Both of them increase. This will increase renal tubule flow. Again though, if you have an
afferent arteriole vasoconstriction, you decrease renal blood flow. You add these 2 together
and you get a less of a change on glomerular filtration if they occur in a minor vasoconstriction
on both sides. This though, however, will still decrease renal blood flow. If, however, you get
a pronounced vasoconstriction, you could start to affect GFR, decreasing it and have even
larger decreases in renal blood flow.