So this is a highly confusing topic. No matter how many times you read it, some amount of doubt is always there in your mind. So an advice to the readers, bookmark this post because you will be needing to read it more than once to get the drift.
First of all, let us review the effects of Angiotensin II on Glomerulus.
It constricts both the afferent and efferent arterioles but preferentially increases efferent resistance. Why? 3 reasons:
1. Efferent arterioles have a smaller diameter in their basal state.
2. Ang II stimulates the release of vasodilator NO from the afferent arteriole.
3. Ang II minimizes vasoconstriction at the afferent arteriole via the stimulation of Ang II type 2 (AT-2) receptors, which result in vasodilatation through a CYP450 dependent pathway.
The net effect of preferential rise in efferent arteriolar resistance is that the glomerular pressure is increased or stabilized(in hypoperfusion states), which helps to maintain or increase GFR. But in the long run, lots of fluid have been filtered out leaving behind the proteins which raise the colloid osmotic pressure, eventually enough to overrule the hydrostatic pressure and hence it leads to decrease in GFR.
Ang II also reduces GFR by causing constriction of the mesangial cells which reduces the effective surface area for filtration.
-VM
all the points are overlapping one another. Can you please repost?
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