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Ok - so i've racked by brain over this and have only come up with a few answers - if any of you would be willing to throw out some other ideas, I would really appreaciate it. Here' the question:
Experimentally, if we reduce the renal perfusion pressure by 15mmHg (think Goldblatt constrictor model) and hold it constant at this level despite changes in the peripheral pressure, how is it possible for the Na output to return to equal the Na intake after a few days (you would think initially that the Na intake would remain higher than the output b/c the kidney is attempting to retian fluid and water to increase it's pressure back to the set point, however because we have isolated and controlled the pressure to the kidney, it is not possible to raise the pressure in the kidney. the renin-angiotensin system is functional and continues to excrete excessively. The other way to think of this question is - what makes it easier for the kidney to excrete salt?
I have come up with the following:
a. It is possible that the itake of Na is reduced in the experimental animal. if this is the case then the pressure that the kidney is seeing is adequate for the lower than normal salt intake to be excreted - thus returning it to normal.
b. another possibility is that b/c of the dramatic increase in Angiotenin, there is an increase in water drinking, and also a dramatic decrease - to undetectable levels - in ADH, both of which will cause increased fluid level and thus water diuresis which may be able to develop despite the controlled low renal perfusion pressure, and thei ncreased water diuresis will cause increased na to be excreted along with it.
c. a third possibility is the addition of a diuretic or some other mechanism that decreases the kidney's ability to concentrate urine (what else will do this????)
d. also - and perhaps far fetched - if the pt somehow developed a secondary pathology such as a renal medullary lesion that reduced the ability to concentrate urine and will allow for the output of Na and water to return to normal, or even development of interstitial nephritis which will cause a salt wasting syndrom and will excrete more salt than would be normally expected.
PLEASE- if you know of anything else, let me know - i have a feeling that i'm missing something obvious. Thanks!
Experimentally, if we reduce the renal perfusion pressure by 15mmHg (think Goldblatt constrictor model) and hold it constant at this level despite changes in the peripheral pressure, how is it possible for the Na output to return to equal the Na intake after a few days (you would think initially that the Na intake would remain higher than the output b/c the kidney is attempting to retian fluid and water to increase it's pressure back to the set point, however because we have isolated and controlled the pressure to the kidney, it is not possible to raise the pressure in the kidney. the renin-angiotensin system is functional and continues to excrete excessively. The other way to think of this question is - what makes it easier for the kidney to excrete salt?
I have come up with the following:
a. It is possible that the itake of Na is reduced in the experimental animal. if this is the case then the pressure that the kidney is seeing is adequate for the lower than normal salt intake to be excreted - thus returning it to normal.
b. another possibility is that b/c of the dramatic increase in Angiotenin, there is an increase in water drinking, and also a dramatic decrease - to undetectable levels - in ADH, both of which will cause increased fluid level and thus water diuresis which may be able to develop despite the controlled low renal perfusion pressure, and thei ncreased water diuresis will cause increased na to be excreted along with it.
c. a third possibility is the addition of a diuretic or some other mechanism that decreases the kidney's ability to concentrate urine (what else will do this????)
d. also - and perhaps far fetched - if the pt somehow developed a secondary pathology such as a renal medullary lesion that reduced the ability to concentrate urine and will allow for the output of Na and water to return to normal, or even development of interstitial nephritis which will cause a salt wasting syndrom and will excrete more salt than would be normally expected.
PLEASE- if you know of anything else, let me know - i have a feeling that i'm missing something obvious. Thanks!
