Kidney physiology interrogate?

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

Thanks surrounded by advance

Answers:
What the previous personality described is a regulatory method of the kidney, but actually it is not the AUTOREGULATORY method. The autoregulatory method is not fully couched, but the overall idea is that the blood vessel bringing blood into the kidney can actually give an account when they are being stretched too much, and they compensate.

The standard formula for this kind of flow is:

P = Q * R

Where P = pressure, Q = kidney blood flow, and R = vascular resistance. The switch point of autoregulation is that you always want to declare 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 maintain kidney blood flow (Q) the same, later vascular resistance (R) must also go up--P and R are directly related! Conversely, if pressure (P) go down, then R must also turn down to keep a constant Q.

Here is an example. Let's utter 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 stumble to compensate. That means that the arterioles will dilate (less resistance) to keep going a constant flow.

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

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

First, afferent and efferent vessels own 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 secure. That increases blood pressure and glomerular filtrate amount.

High amount of glomerular filtrate will be registered as high sodium height in the macula densa, downregulating that piece of equipment.

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Kidney physiology interrogate?

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