Alcohol Acts As A Diuretic Biology Essay

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AVP is created in the hypothalamus and is up regulated during times of decreased water intake, or if the ion concentration in the blood is too high (Svane, Thorn, Richter, & Mohr, 1995). Interestingly, when the ion concentration is too low, the hypothalamus produces less AVP mRNA and also decreases the length of the poly A tail of the mRNAs that it does make (Svane et al., 1995). This shortening of the poly A tail likely allows the mRNAs to be degraded faster and thus translate into fewer AVP molecules. AVP is stored in the posterior pituitary gland until it is required (Zhao, Nijland, Ervin, & Ross, 1998). After being released into the blood AVP binds to its receptor, V2, which is expressed in the kidneys (Deen et al., 1994). V2 is a G-protein coupled receptor that activates adenylate cyclase (Henn et al., 2005). In turn adenylate cyclase activates cAMP which then activates PKA (Henn et al., 2005). PKA then phosphorylates aquaporin-2 (AQP2) that is present in the cytoplasm (Henn et al., 2005). Phosphorylated AQP2 is then able to insert itself acroos the plasma membrane and thus allows water to enter into the cell (Henn et al., 2005). This occurs in the cells that line the nephrons in the kidney and thus allows greater water reabsoroption in the kidneys. Since activated PKA is capable of phosphorylating a number of different proteins, there must be some way that it is capable of phosphorylating only AQP2 when AVP binds to V2 to begin signal transduction. Interestingly, Henn et al. (2005) have shown that there are a group of proteins known as A-kinase anchoring proteins (AKAPs) which play a major role in the specificity that occurs in this pathway. They suggest that these AKAPs compartmentalize the cell. This is supported by their results which showed that increased PKA alone did not activate AQP2, whereas increased PKA in the correct location was able to (Henn et al., 2005). Therefore, these AKAPs must ensure that AVP initiated signal transductions, which eventually activate PKA, lead only to the phosphorylation of AQP2 and none of PKAs other downstream targets.

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Next I will describe how alcohol affects this pathway. It has been known for a long time that alcohol is a fast acting diuretic, causing increased excretion of water (Murray, 1932). Upon initial intake of alcohol, it has been found that levels of AVP in the blood decrease and directly relates to decreased ion concentration in urine (Eisenhofer & Johnson, 1982). This suggests that alcohol is likely inhibiting the release of AVP, rather than binding to AVP to inhibit it. Over time, however, the concentration of AVP in blood increases, but this does not correlate with blood alcohol levels decreasing (Eisenhofer & Johnson, 1982). For some reason, these increased levels of blood AVP do not lead to increased ion concentration in urine as would be expected {{49 Taivainen,H. 1995}}. This has led Taivainen et al. (1995) to predict that alcohol could also act in a way that desensitizes the receptors or that alcohol has some other effect that alters water uptake in the kidneys. Finally, there is a period after drinking, after blood alcohol levels have greatly reduced when the increased AVP levels lead to very strong antidiuresis {{49 Taivainen,H. 1995}}. This can be so strong that it actually reverses the initial dehydration and dilutes the blood beyond normal levels {{49 Taivainen,H. 1995}}. Although there is not a known mechanism for how alcohol acts as a diuretic there is evidence that alcohol initially inhibits AVP output. Thus, AVP cannot enter the blood stream and therefore cannot bind V2 to begin signal transduction in order to move AQP2 into the plasma membrane and in this way the kidneys are unable to reabsorb as much water as normal. This results in dilute urine and temporary dehydration. It seems that the body responds to this dehydration by stimulating a lot of AVP, but while alcohol is still in the blood this does not reverse dehydration. However, once alcohol concentrations go down, AVP can act properly, but the high levels that were released during dehydration often over compensate and result in diluted blood. This over dilute blood is a concern in alcoholics that are withdrawing from alcohol. Under normal conditions alcoholics suffering alcohol withdrawal have AVP levels in blood that are about twice that of normal controls {{59 Emsley,R.A. 1987}}. Therefore, when alcohol is not present in order to counteract these high AVP levels, the patient often suffers from overhydration{{51 Eisenhofer,G. 1985}}.

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Alcoholics suffering alcohol withdrawal have previously been treated with intravenous fluid and electrolyte therapy due to the knowledge that alcohol acts as a diuretic {{51 Eisenhofer,G. 1985}}. However, this is likely ineffective or even potentially counterproductive due to evidence showing that these patients actually retain higher amounts of water than normal. It seems that a potential way to reduce the effects of overhydration would be inhibit AVP by have another molecule bind to it in the blood stream so that it cannot function as an antidiuretic. This molecule could then be gradually taken away until the body begins to release an appropriate level of AVP. The effect of this would be similar to slowly reducing alcohol intake, but would not have the toxic effects of alcohol and also would not run the risk of having the patient over consuming again.

Above I have described the pathway that AVP follows in order increase water uptake from the nephrons in the kidneys. This pathway is made much more complex when alcohol consumption is concluded. Alcoholics often have too much AVP in their blood to counteract the regular alcohol intake, however, during alcohol withdrawal, these levels are too high and this can lead to overhydration. I have described a potential treatment above which might help to decrease symptoms of alcoholics that are trying to quit drinking.

Word Count without citations =1019

At total word count of 1108

Personal Reflection (Written Summary)

For this problems summary I was unable to start as early as in the past. It was interesting because the main pathway that is used to activate the aquaporins in the kidney seemed quite simple, however, the effects of alcohol made this problem summary much more complex than it seemed at first. I did find it interesting however that sustained alcoholism actually leads to increased water intake. Having known that alcohol is a diuretic I would have thought that a lot of alcohol would potentially lead to severe dehydration rather than overhydration. Overall, I learned a lot about the AVP signaling pathway, but I feel that there is still a lot to be known about the effects that alcohol has on water balance.

Personal Reflection (Group Presentation)

From our group presentation I learned about the varied effects that alcohol can have on the body. Although a quick search made it seem like alcohol caused dehydration, a more complex relationship was discovered. I found that the group presentation was fun to make and really got me interested into some of the mechanisms involved in alcohol consumption.

Personal Reflection