Diuretics

[endlesslove]

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Hey guys, what's a good (legitimate) website that describes how diuretics like caffeine increase urine output (in terms of sodium and potassium excretion) or if you want, you can explain it to me.

Thanks

 

[DHG]

Hey guys, what's a good (legitimate) website that describes how diuretics like caffeine increase urine output (in terms of sodium and potassium excretion) or if you want, you can explain it to me.

Thanks

This may be too elementary, but here anyways:
http://www.e-kidneys.net/diuretics.html

 

[TMVegas]

I don't have anything in my notes about sodium/potassium secretion, but here is what I have on caffine:
Caffine causes vasoconstriction which increases vascular pressure;
this increases blood pressure which raises glomerular capillary pressure;
more filtrate enters tubule, more urine is produced

 

[endlesslove]

which of these five categories of diuretics does caffeine belong in:

carbonic anhydrase inhibitors
loop diuretics
thiazide diuretics
osmotic diuretics
potassium-sparing diuretics

?

 

[TMVegas]

My A&P book lists it as a xanthine

P.S. it also says xanthines influence the nephron by decreasing Na and Cl reabsorption

 

[yatzek]

its in the class of "naturally occuring diuretics".. it inhibits Na reabsorption in the proximal tubule (so water doesnt follow)
it also works by slowing down gfr... ethanol is also in this class but its moa is by inhibitting secretion of adh (vasopressin)...

i was studying vasopressin recently and it plays a huge role, when you wake up and soon afterwards need to pee (but didnt need to pee all night) its because vasopressin is secreted when you sleep.. anyway im drifting off subject- is it just me or doesnt everyone think knowing this stuff is cool?

 

[endlesslove]

i'm confused:

if adenosine is a vasoconstrictor on the afferent arterioles, and caffeine is an adenosine receptor antagonist, it would seem like caffeine's inhibition of adenosine's vasoconstrictive properties would produce an overall vasodilatory effect but that is not the case. instead, caffeine is a vasoconstrictor. how is this possible given that caffeine antagonizes the adenosine receptor?

 

[rxgal8]

i'm confused:

if adenosine is a vasoconstrictor on the afferent arterioles, and caffeine is an adenosine receptor antagonist, it would seem like caffeine's inhibition of adenosine's vasoconstrictive properties would produce an overall vasodilatory effect but that is not the case. instead, caffeine is a vasoconstrictor. how is this possible given that caffeine antagonizes the adenosine receptor?

Vasodilation at afferent arteriole due to low adenosine should increase GFR (glomerular filtration rate), so I'm not sure how that leads to an increase in urine output.

But caffeine does reduce Na reabsorption and since water follows salt, less water reabsorption occurs, leading to an increase in urine.

edit: high GFR will increase urine output.

 

[endlesslove]

Vasodilation at afferent arteriole due to low adenosine should increase GFR (glomerular filtration rate), so I'm not sure how that leads to an increase in urine output.

But caffeine does reduce Na reabsorption and since water follows salt, less water reabsorption occurs, leading to an increase in urine.

another poster, tmvegas, said vasoconstriction leads to increased glomerular filtration. so what's the consensus? vasoconstriction or vasodilation? (I get the sodium absorption part...caffeine 1) increases GFR 2)decreases Na reabsorption). i knew i shouldnt have just accepted my pharmacology professor's "caffeine is a diuretic" statement last yr and asked him to explain the physiological mechanisms =(. now it's too late.

 

[rxgal8]

another poster, tmvegas, said vasoconstriction leads to increased glomerular filtration. so what's the consensus? vasoconstriction or vasodilation? (I get the sodium absorption part...caffeine 1) increases GFR 2)decreases Na reabsorption). i knew i shouldnt have just accepted my pharmacology professor's "caffeine is a diuretic" statement last yr and asked him to explain the physiological mechanisms =(. now it's too late.

Well, this is how I learnt it:

Vasodilation at "afferent" arteriole via low adenosine causes an increase in GFR.

Vasoconstriction at "efferent" arteriole via renin causes an increase in GFR; because constriction (smaller diameter) means higher resistance and thus, less blood flows out of the glomerulus due to a high glomerular hydrostatic pressure, which eventually leads to an increase in GFR.

I take what I said back, the high GFR will then lead to an increase in urine output.

 

[ZpackSux]

Caffeine is a Xanthine derivative.. like Theophylline..

Goodman and Gillman is a great book for this sort of pharmacology questions.

Good lord...the last time I thought about this was in 1992..pharmacology class.

 

[VCU07]

GFR cannot rise much above 120ml/min...inc. GFR may increase the amount of urine produced and excreted, but that also depends upon the ion concentrations within our bodies. For example, when our bodies have enough or more than enough Na (hypernatremic) we will retain more fluid to dilute the sodium to maintain osmotic balance. Also, renin will not specifically cause vasoconstriction at the efferent arteriole. It will cause general vasoconstriction, which will inc. our blood pressure in case of hemorrage or other cause. If you remember from physiology, another compensatory mechanism is the barro receptor system.

Well, this is how I learnt it:

Vasodilation at "afferent" arteriole via low adenosine causes an increase in GFR.

Vasoconstriction at "efferent" arteriole via renin causes an increase in GFR; because constriction (smaller diameter) means higher resistance and thus, less blood flows out of the glomerulus due to a high glomerular hydrostatic pressure, which eventually leads to an increase in GFR.

I take what I said back, the high GFR will then lead to an increase in urine output.

 

[ButlerPharm.D.]

The following has a PowerPoint presentation I think you might find quite interesting in regards to your questions.
http://www.science.mcmaster.ca/biopharm/ppt/caff.ppt#267,15,ADENOSINE

i'm confused:

if adenosine is a vasoconstrictor on the afferent arterioles, and caffeine is an adenosine receptor antagonist, it would seem like caffeine's inhibition of adenosine's vasoconstrictive properties would produce an overall vasodilatory effect but that is not the case. instead, caffeine is a vasoconstrictor. how is this possible given that caffeine antagonizes the adenosine receptor?

 

[neonam11]

K, this is the tidbit that I learned:

Caffeine is a xanthine and it does 2 things that may increase urine output. First, it does cause vasodiation at the AFFerent arteriole. If there is less resistance at the afferent arteriole, then GFR would increase, more blood would be filtered through the Bowman Capsule. The second thing that it does is that, yes, it does inhibit NaCl reabsorption, whether at the ascending Loop of Henle of distal convulated tubule, I don't know (although I would think that it's at the distal convoluted tubule since inhibition at the ascending loop of Henle would cause a loss of potassium as well as NaCl which is not the case). Since more Na is retained in the lumen of the nephron, more water would be retained and excreted as well. Probably it is due to the latter mechanism more than the increase in GFR that makes drinking caffeine makes you pee so often.

Some minor points: 1) vasodilation at the EFFerent arteriole would decrease GFR, but as I said, caffeine is a vasodilator at the AFFerent arteriole to increase GFR 2) Angiotensin II (not renin cuz renin is an enzyme that cleaves angiotensinogen which then forms angiotensin I which is then cleaved by ACE to form angiotensin II) causes vasoconstriction at the EFFerent arteriole. Yes, angiotensin II does cause vasoconsitriction in the systemic blood vessels, but for the arterioles of the kidney, it causes vasoconstriction only at the efferent end as far as I know.

 

[npage148]

Yes, angiotensin II does cause vasoconsitriction in the systemic blood vessels, but for the arterioles of the kidney, it causes vasoconstriction only at the efferent end as far as I know.

AG2 will cause vasoconstriction of both the efferent and afferent artioles but postiglandins will casue vasodilation of the afferent artioles cancelling the affecte of AG2. Thats why NSAIDS will reduce renal blood flow and possible kindey damage in high risk people. It will stop the vasodilitory PGE synthines and AG2 will provail

 

[neonam11]

AG2 will cause vasoconstriction of both the efferent and afferent artioles but postiglandins will casue vasodilation of the afferent artioles cancelling the affecte of AG2. Thats why NSAIDS will reduce renal blood flow and possible kindey damage in high risk people. It will stop the vasodilitory PGE synthines and AG2 will provail

Hmmm, that's not what it says in my Koda-Kimble text. According to p. 31-8, angiotensin II causes EFFerent arteriole vasoconstriction as well as systemic vasoconstriction. You are correct in stating that NSAIDS and and COX II will inhibit prostaglandin release at the AFFerent arteriole which can lead to acute renal failure if it is constricted badly enough.

 

[npage148]

Hmmm, that's not what it says in my Koda-Kimble text. According to p. 31-8, angiotensin II causes EFFerent arteriole vasoconstriction as well as systemic vasoconstriction. You are correct in stating that NSAIDS and and COX II will inhibit prostaglandin release at the AFFerent arteriole which can lead to acute renal failure if it is constricted badly enough.

Goodman and Gillman states on page 819 of edition 10 that it will affect both aritoles beds along with the permability of bowmans capsule

 

[neonam11]

Goodman and Gillman states on page 819 of edition 10 that it will affect both aritoles beds along with the permability of bowmans capsule

So I asked my pharmacology professor and, yes, he said that angiotensin II does constrict both the AFFerent and EFFerent arteriole. However, he doesn't know to what the magnitude of vasoconstriction is for angiotensin II has on either side, whether if it's the same or unequal.

The reason why I thought Koda-Kimble was correct is because some ACE inhibitors have the potential of causing acute renal failure. By taking ACE inhbitors, there is less angiotensin II produced, and you would have vasodilation at the EFFerent end, causing GFR to decrease. This leads to acute renal failure. Perhaps if angiotensin II works on both ends, the theory still works; it perhaps works to a greater extent on the EFFerent end. If you take an ACE inhibitor, you would have vasodilaton on both the AFFerent and EFFerent end, but since vasodilation is greater at the EFFerent end, you have a net decrease in GFR. Well, that's my two cents. Hope you are all digging pharmacology as much as I am.

 

[npage148]

Im guessing that it is more active on the efferent end but im not sure and ive looked for about 30 min for the answer and i came up empty handed. Im probabaly just pretty bad at using hubnet. I do enjoy therapeutics, its probabaly my favorite class behind kinetics.