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In practice, when you have vasoconstriction of the glomerular capillaries and subsequently an increase in blood pressure, glomerular filtration rate increases. However, this seems counterintuitive to Bernoulli's principle.

During vasoconstriction, because the radii of the capillaries are getting smaller, we should expect an increase in flow rate and blood velocity. According to Bernoulli's principle, the outward hydrostatic pressure should drop.

How does this lead to an increase in filtration rate?

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up vote 4 down vote accepted

The previous answer isn't quite correct, because, well, blood flow is complicated and the body has autoregulatory mechanisms. As Alex mentioned, vasoconstriction doesn't occur in capillaries because they lack a muscle layer. It does occur in the small arterioles before and after the glomerulus (the afferent and efferent arterioles, respectively).

Bernoulli's principle mainly applies to larger arteries and arterioles, and not capillaries. Capillaries are so tiny that the red blood cell is a significant portion of the diameter, so the assumption of no viscosity is no longer valid. See this discussion for an explanation.

To address your question, here's a basic picture of the glomerulus, from Gray's Anatomy. image

The afferent arteriole is in red, and the efferent arteriole in blue. The glomerular filtration rate (GFR) depends on the pressure difference between the two, which affects the hydrostatic pressure at the glomerulus. Also, note that vasodilation has the opposite effect of vasoconstriction on GFR. (For a nice image and explanation, look at Figure 6 here) So:

  • Constriction of the afferent arteriole decreases the blood flow into the glomerulus and thus the glomerular hydrostatic pressure, which leads to a decrease in GFR.

  • In contrast, constriction of the efferent arteriole decreases blood flow out of the glomerulus, and this increases the glomerular hydrostatic pressure and leads to an increase in GFR.

Both the afferent and efferent arterioles are regulated through hormones (and drugs that inhibit the hormones). Prostaglandins dilate the afferent arterioles, and NSAIDs inhibit this action. Angiotensin II preferentially constricts the efferent arteriole, and this action is restricted by an ACE inhibitor. (Source: First Aid for the USMLE Step 1)

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It's worth noting that the afferent arterioles are significantly larger than the efferent arterioles, which creates the high-pressure environment required for filtration in the first place. – Armatus Jul 29 '12 at 9:28

To my knowledge, capillaries in general and the renal capillaries in glomeruli in particular do not have muscle cells to constrict. The latters have only a basal layer with podocytes lying directly on it (link to the open textbook).

Therefore, the vasoconstriction takes place only in arterioles before the glomeruli, and this vasoconstriction leads to the increased hydrostatic pressure which propagates to the glomerular cappilaries. The blood flow rate and velocity do not change, therefore the increased hydrostatic pressure works against the constant pressure of Bowman's capsule and osmotic pressure of the colloid medium, leading to the increased net filtration pressure (NFP). Filtration rate and filtration pressure are directly connected, so that the rate increases either.

For more details, please, refer to the textbook I provided the link to above.

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