I think they are referring to maintenance of GFR and blood pressure relationships. Ergo the mentioning of the renal function. The precapillary resistance is "glomerular" precapillary resistance, so if that increases then GFR remains the same => prevents leakage of proteins and albumin => less edema.
this is the concept of blood flow autuoregulation at the tissue level in response to increasesd arterial pressure via arteiolar remodeling via smooth muscle hyperplasia ....
precapillary resistance = describing the arterioles. he's got minimal protein in the urine; and no albumin. the key was paying attention to the blood pressure. Pressure is regulated by the resistance vessels as boards calls it which is the arterioles aka precapillary resistance.
I've been searching for my source for this but can't seem to find it. However, the way I thought about it was that edema happens via the capillaries. If there is increased resistance via the precapillary sphincters as much blood wouldn't be able to get into the capillaries. The blood would instead get shunted via anastomoses to the veins. This article from cvphysiology.com explains it a little better: CV Physiology: Tissue Edema and General Principles of Transcapillary Fluid Exchange
Maybe the question is dealing with the concept of myogenic arteriolar vasoconstriction which is a another anti-edema mechanism. The pre capillary sphincter contract in response to a raise in BP. I got the Q wrong because I picked lymphatic flow. They love to go for the "what else" element of any topic. I cannot find any reason why the lymphatic option could be wrong :/
https://www.ncbi.nlm.nih.gov/books/NBK53445/?report=classic Check the figure 4.1 The Margin of Safety Against Edema Formation โ Edema Safety Factors
In addition to what has already been said I think an important point in the question was regulatory adjustments which points more towards arteriolar regulation.
https://d1yboe6750e2cu.cloudfront.net/i/0b2159dfcfd96ee300a97e2e07d7d0c0229a2d3f
"When arterial pressure falls, myogenic tone is reduced in arterioles, decreasing their resistance to flow and maintaining capillary pressure. These observations suggest that capillary pressure may be regulated over the same range of pressure changes over which flow is autoregulated in a given organ. Indeed, from the relation:"
https://www.ncbi.nlm.nih.gov/books/NBK53445/
why is plasma oncotic pressure wrong?
A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.
Aortic Diastolic Pressure
Aortic Systolic Pressure
I also think that the point being made here is about mean arterial pressure (MAP), which is what autoregulatory systems actually change based on. Because he has increased MAP (due to increased DBP), the capillaries will constrict to maintain constant pressure/flow through the capillary bed.
i don't think you need to think all that much. look at all the options and think of what happens when they increase. A, B, C, D and F all can cause interstitial edema. But increasing precapillary resistance definitely doesn't.
1. Aortic Diastolic Pressure
1. High TPR = high DP
2. High HR = high DP
3. High SV = high DP
2. Aortic Systolic Pressure
1. High Contractility = high SP
2. High SV = high SP
3. Low Compliance = high SP
submitted by โferrero(48)
A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.