Glomerular Filtrate: Angiotensin II and Glomerular Filtration Rate

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[@fionayange]

Thank you for the simplest but yet very understandable video which took me ages to understand.

[@LanceMillerPhD]

Thanks, I’m glad you found it helpful

[@Christmas7731]

This channel is AMAZING! Instant subscribe! I'm a graduate in Physiology studying Medicine now and is so easy to forget little details like this. These videos are perfect for a quick and accurate reminder! Thank you!

[@dannyfeldman2448]

Gotta take this off. Net effect of Angiotensin II is preferential vasoconstriction of EFFERENT arterioles. This INCREASES GFR as the sole survivor mechanism in cases of low BP. Sympathetic nervous system activates alpha 1 and beta 1 receptors in the kidneys. 1. alpha 1 is present in EA and AA-> vasoconstriction 2. Beta 1 is present on JG cells causing renin secretion renin-> Angiotensinogen to AT I -----------> AT II via ACE ----------> EA Constriction Net effect in low BP States on GFR is INCREASE but more appropriate "PRESERVE" GFR before it truly gets destroyed from low perfusion.

[@ricardotorres8114]

right bro 👌

[@emilyi771]

Thank you, Dr. Miller. This helped a lot.

[@noahmarcus7817]

Calcium doesn't cause contraction in smooth muscle by binding actin...

[@raffaerer]

by binding troponin

[@nvnoveritas]

@@raffaerer no, not in smooth muscle

[@colesonksen5003]

@@nvnoveritas yes it does "Smooth muscle contraction is due to the interaction of myosin filaments with thin filaments. Thin filaments are composed of actin, tropomyosin, caldesmon, and calmodulin in ratios 14:2:1:1. Tissue-specific isoforms of actin and beta tropomyosin are expressed in smooth muscle."

[@colesonksen5003]

calcium activates myosin light chain kinase which causes phosphorylation of myosin and allowing it to interact with actin

[@noahmarcus7817]

@@colesonksen5003 looks like you finally found the right answer. Calcium>>calmodulin>>activation of MLCK>>phosphorylation of regulatory light chain on myosin>>initiation of cross bridge cycle

[@javeriaiqtidar1302]

Thank you so much!

[@saeeda4517]

what is this bullshit, i thought AT2 increases GFR not decrease it

[@thecoreybrown]

You're right, it would if you had low levels of AT2 which would constrict only the efferent, but if you had high levels of AT2 you would have a decrease in GFR from constricting both afferent and efferent.

[@aymenyousfi447]

thanks 😊

[@LanceMillerPhD]

You're welcome!

[@timothymcnamara1908]

Hi, The next video in this series (tubuloglomerular feedback) mentions that an increased GFR (and thus NaCl concentration) will eventually result in the inhibition of renin release. This would then result in a decrease in angiotenin II and thus (according to this video) a further increase in GFR. This doesn't seem correct however I'm finding mixed explanations everywhere. Is anybody able to explain?

[@subhodiproy536]

Timothy McNamara Bro, as far as I know Angiotensin II increases GFR.

[@Eman1900O]

Ang II increases GFR because although it constricts both afferent and efferent arterioles, it has preferential constriction on the efferent arteriole, which would increase GFR

[@yasser5609]

Traditionalist that’s at normal condition by back it from low to normal. “By in high concentration Ang II decrease GFr “will act on Mesangial cell for promote it contract and thus decrease “the capillary surface area of filtration” and thus decrease Kf that’s lead to decrease GFR. I hope you’re understanding 🌺

[@cyrilsl9841]

@@yasser5609 so raas decrease gfr?

[@p_HoE_niX]

@@cyrilsl9841 so what's the point of RAAS, it's basic point was to increase urine output, why it's decreasing? Have same doubt as you.