Step I question about capillary hydrostatic pressure

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cuber101

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10+ Year Member
Hey all,

In the Kaplan Lecture notes it says that capillary hydrostatic pressure is increased by arteriolar dilation and is also mentioned by Conrad Fischer in the videos. However, he also goes onto mention when discussing ACE inhibitors that they dilate the arterioles and hence decrease capillary hydrostatic pressure and prevents extravasation of fluid. How does this make sense?

Thanks in advance
 
Afferent arteriolar dilation leads to more flow into the glomerulus leading to increase cap hydrostatic pressure. That is what he is initially explaining. Angiotensin II acts as a vasoconstrictor, but preferentially on the efferent arteriole. So by blocking ACE you decrease efferent arteriole constriction (dilate) thereby decreasing Cap HP by decreasing the pressure gradient between afferent and efferent arterioles leading to decreased glomerular flow.
 
ACE-I leads to widespread arteriolar dilatation which leads to more blood being pooled in the veins which explains why overall BP drops.

If only particular arterioles are dilated, like, say leg muscles during running due to local metabolites, but the overall system has stayed relatively the same, then hydrostatic pressure will increase in those capillaries.

If the Kaplan guy was just talking about renal arterioles then the above explains that.