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 blow 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 graph that you see,
where you have mean arterial pressure on the X-axis,
and blood flow on the Y-axis.
There’s a range at which this 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 that happens.
If you have too much sheer stress across a vessel,
it may cause it to constrict.
If there’s not enough sheer stress, it will cause it to dilate on its own.
So those two 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 graph,
so we’re going to use renal tubular feedback in more of a diagram form.
So as we look for glomerular tubular feedback,
let’s talk through the two 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 flowmeter in your kidney
and determine how fast the fluid is traveling through it.
So what the body does instead is sense the amount of sodium chloride in bulk form
that’s transferred across the renal tubule.
If there are high amounts 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’s a little signal that sent 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 arterial to constrict
and the efferent arterial 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 a low sodium chloride, you’re going to get a block of adenosine.
You will, however, increase more renin.
As you increase more renin from these juxtaglomerular cells,
what this does is increases angiotensin I and 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,
the net result is tubule 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 diagram of trying to look at glomerular filtration rate there on the bottom,
and then renal blood flow with its autoregulatory zone,
what other molecules affect renal blood flow?
Nitric oxide and prostaglandins, especially prostaglandin E2,
cause dilation of blood vessels, and therefore, more renal blood flow.
The endotheliums and leukotrienes cause a constriction.
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 angiotensin II,
you get a decrease in renal blood flow and glomerular filtration rate.
Atrial natriuretic peptide or ANP causes an increase in renal blood flow.
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.