Kidney physiology question?

Question

Can someone explain the autoregulatory function of the kidneys to keep renal blood flow and GFR relatively constant even from a change in pressure between 75-160 mmHg?

Thanks in advance

Answer 1

What the previous person described is a regulatory method of the kidney, but actually it is not the AUTOREGULATORY method. The autoregulatory method is not fully understood, but the overall idea is that the blood vessels bringing blood into the kidney can actually tell when they are being stretched too much, and they compensate.

The general formula for this kind of flow is:

P = Q * R

Where P = pressure, Q = kidney blood flow, and R = vascular resistance. The key point of autoregulation is that you always want to maintain a CONSTANT FLOW (Q) to the kidney. So looking at the equation, you can see that if pressure (P) goes up, and you want to keep kidney blood flow (Q) the same, then vascular resistance (R) must also go up--P and R are directly related! Conversely, if pressure (P) goes down, then R must also go down to keep a constant Q.

Here is an example. Let's say your systolic blood pressure (for some reason) falls from 120 to 75. Your kidneys want to maintain a constant blood flow. So since the pressure falls from 120 to 75, the vascular resistance must also fall to compensate. That means that the arterioles will dilate (less resistance) to maintain a constant flow.

On the other hand, if your blood pressure suddenly jumps from 120 to 165, your vascular resistance will increase (the arterioles will constrict), to maintain a constant Q. Look back at the equation and realize the relationship between P and R, when you want to keep Q constant.

In the end, autoregulation has to do with the second-to-second regulation of BLOOD FLOW (Q) into the kidney. The RAA system described by the previous poster occurs over a matter of days and is responsible for moderate-term blood pressure (not flow) regulation. The RAA system is not autoregulation.

Answer 2

1

Answer 3

2

Answer 4

First, afferent and efferent vessels have muscle and can contract or relax.

Second, macula densa (or dense spot) is sensitive to sodium.

Third, there are forces inside of the glomeruli, hidrostatic and coloidosmotic. Hidrostatic tend to filtrate, coloidosmotic tend to retain filtrate.

Low amout of glomerular filtrate is detected as low sodium and an increase of renin release, that triggers renin- angiotensinogen to angiontensin 1- ACE -angiotensin 1 to 2 -aldosterone chain. That increases blood pressure and glomerular filtrate amount.

High amount of glomerular filtrate will be registered as high sodium level in the macula densa, downregulating that mechanism.

Answer 5

Can you give me a definition of traced? I am not familiar with that term.