I get that AngII preferentially binds to the efferent arterial causing greater pressure in the glomerulus and thus increased GFR. Why though would your body want to increase GFR?
If you have low volume triggering renin release, why would you want to increase the amount being filtered? this seems counter-intuitive
Hey nm825,
This is a good concept to tie down because it's a great tie in for multiple pathologies (i.e. diabetes, HTN) along with the reason why patients are given ACE-i. I'm a big sports fan and the kidneys are like Kobe Bryant in my mind. They're tremendously hard working but also selfish to the same extent, which is what the body needs for good health.
I think it helps to think of the kidney as a sponge with an incoming hose, representing the afferent arteriole, feeding into the sponge and a hose draining the kidney, which represents the efferent arteriole. When there is a hypovoemic state and the kidney isn't seeing enough blood, its next step is activation of the RAS. This not only increases perfusion to BOTH kidneys but the angiotensin effect also constricts the efferent arteriole.
So, imagine that more volume is coming in, or at the very least at an increased pressure than usual (RAS increases bp) but the outcoming hose is narrowed or slightly clamped down. Being that the sponge (kidney) is healthy it will see more blood at an increased rate and be able to filter it well, which is why the GFR increases. However, eventually the sponge begins to be worn out and begins to slough off and wither away since it's been so overworked. This occurs in a more advanced disease state and is represented by a decreased GFR. This is why patients who are either hypertensive or diabetics (often both if they're diabetic) need to be placed on an ACE-i to try and salvage the kidneys for as long as possible and prevent failure. ACE-i mess with the RAS, which eases the constriction/clamp on the efferent arteriole. Thus, easing the brunt of the force on the sponge/kidney.
Also, why's it important that the RAS increases blood flow to both kidneys? Because if there is a clot in the L renal artery, the L Kidney will activate RAS even though the R kidney is perfectly perfused and happy. Over time, the R kidney is worked into the ground and starts to fail.
So how are the kidneys like Kobe? Sometimes it wants to work so hard and wants to ensure that it receives ample blood that it'll damage the team and even harm the other kidney--like getting Shaq traded to Miami lol. Kobe probably didn't want to pull the lakers apart but was selfish enough that a byproduct was what had happened. RAS activation will always lead to constriction of the efferent arteriole via angiotensin as a byproduct, which will eventually lead to badness. The kidneys are awesome and Kobe is great (but MJ is GOAT), and I hope this clears it up for you.
