so clearly the question is getting at GFR. We want net reabsorption in hypotension situations so the question wants us to find what causes net filtration.
Vasoconstriction of precapillary resistance arterial was causes decreased GFR. A decreased GFR results in increased reabsorption. This is because hydrostatic pressure drops, leading to capillary oncotic pressure driving fluid into the capillary.
Decreased osmotic pressure results in net filtration due to the hypo-osmolar pressure. Think about hypertonic solutions. Water leaves the hypo-osmolar RBC to try and equilibrate. This is what I think the answer might be.
Venoconstriction of the post-capillary venules is essentially the same concept as congestion in CHF. It leads to back-up and ultimately increased GFR. Think about putting a knot in a hose and then poking a hole in the hose near the water valve. Water is going to leak out. I also think this would be an acceptable answer.
Reduced capillary hydrostatic pressure causes net reabsorption. This is what we want. So the answer cannot be this.
E is pretty self-explanatory. You are getting net reabsorption of fluid from interstitium to the capillaries.
The question is poorly phrased. So unless I'm missing something.. B&C have to be correct. I would choose B most likely because venoconstriction (C) will eventually lower GFR filtration to the point that you have no net filtration. Think about completely closing the venule.
Pretty sure this question wasn't "clearly" asking about GFR, at all actually. Vasoconstriction of post capillary venules is one of the major reasons why humans are able to survive (at least initially) with a massive loss of blood.
Vasoconstricting arterioles = increase SVR = maintain BP and thus CO to maintain perfusion to vital organs
Vasoconstricting post capillary venules = massive increase in venous return/ venous blood stores into our systemic circulation.
While I definitely agree renal afferent arteriole constriction is definitely important in maintaining volume status, I'm pretty sure renal venules very little role in GFR control - they're so downstream thanks to the unique renal vascular organization, and I'm pretty sure it would be counter intuitive to the rest of our bodies innervation if they were able to be regulated by the same sympathetic mechanisms as everything else. I've actually never even heard of that being a thing (but someone feel free to correct me if I'm wrong).
The organization of the SNS in terms of innervation of our vascular system makes sense from a design point of view. Lots of adrenergic receptors on all vessels except cerebral and coronary. Increase SVR/BP, increase systemic volume, decrease GFR (and also net renin release ---> ANG II effects + aldosterone effects), all to increase volume, CO, and thus blood flow/perfusion to the two organs that matter the most.
Anyway, answer should be B without a doubt.
