bigballer27

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it seems pretty simple in my book, but the questions always seem to ask complicated stuff about ADH and aldosterone that i get wrong, and the relation of the kidney to all these things. can someone please clarify the kidneys role in

1. blood pressure
2. blood volume
3. blood osmolarity
4. ADH/ALDOSTERONE


ughh these things are confusing me....lol thanks for anyone who can help
 
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when is your MCAT test?

I thought renal physiology was among the hardest organ systems to get down. There's no way to summarize it concisely AND address all the potential tough question out there.

All else equal, higher blood volume leads to higher blood pressure --> pressure natriuresis. Blood osmolarity is generally regulated by the osmoreceptors and the thirst mechanism. ADH is one of the key hormones used to regulate osmolarity.

Renin-> Angiotensin II -> Aldosterone leads to electrolyte and water reabsorption.

The above does not attempt to simplify all the complex workings of the nephron.
 
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bigballer27

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when is your MCAT test?

I thought renal physiology was among the hardest organ systems to get down. There's no way to summarize it concisely AND address all the potential tough question out there.

All else equal, higher blood volume leads to higher blood pressure. Blood osmolarity is generally regulated by the osmoreceptors and the thirst mechanism. ADH is one of the key hormones used to regulate osmolarity.

Renin-> Angiotensin II -> Aldosterone leads to electrolyte and water reabsorption.

The above does not attempt to simplify all the complex workings of the nephron.
im taking it may 1st...hope its not too soon lol i have 6 weeks i guess

yeah so , increased osmolarity means lower blood volume and lower BP?

how do the afferent and efferent capillaries work? do afferent take blood away from the glomerulus and lead to highly concentrated blood, which will reabsorb water, etc... from the PCT? not sure if i have that right or not
 

bigballer27

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ooops actually it might be the efferent arterioles and they go away from the glomerulus but not sure how they work...
 
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Increased osmolarity does not necessarily mean lower or higher volume. They're related but different. Context sensitive.

Afferent arterioles encounter blood before it enters the glomerulus, and efferent after it leaves the glomerulus. Constriction of afferent will reduce flow and pressure of blood into the glomerulus and reduce filtration. Constriction of efferent by angiotension II leads to mixed results depending on how much constriction and what's going on with afferent. I would consult with Ohm's Law where Flow = (Afferent Pressure - Efferent Pressure)/Resistance.
 

bigballer27

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Increased osmolarity does not necessarily mean lower or higher volume. They're related but different. Context sensitive.

Afferent arterioles encounter blood before it enters the glomerulus, and efferent after it leaves the glomerulus. Constriction of afferent will reduce flow and pressure of blood into the glomerulus and reduce filtration. Constriction of efferent by angiotension II leads to mixed results depending on how much constriction and what's going on with afferent. I would consult with Ohm's Law where Flow = (Afferent Pressure - Efferent Pressure)/Resistance.
ok i guess thats a simpler way to look at it that helps maybe il look online and wikipedia for some more info

i have repeatedly heard that kidney is a major tested topic on the mcat, so i just want to have it down cold
 

Charles_Carmichael

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Here's a previous post of mine regarding the differences between the ADH and RAAS systems:

The way I think about it, ADH secretion is primarily regulated by osmolarity. There are osmoreceptors in the hypothalamus that detect plasma osmolarity; if osmolarity increases, ADH secretion is stimulated (and you also become thirsty) so that you can reabsorb water to restore osmolarity.

I think of aldosterone more in the sense of body fluid volumes and systemic pressure. If you are hypotensive, the renin-angiotensin-aldosterone system (RAAS) is activated due to a decrease in GFR. This decrease in GFR stimulates renin secretion which ultimately leads to aldosterone secretion and Na+ reabsorption and thus, increases body fluid volume and pressure.

Aldosterone causes reabsorption of Na+ at the distal tubule but it has no direct effect on water reabsorption. What it does though is that it increases the blood osmolarity due to an increased reabsorption of Na+ (this reabsorption is NOT isosmotic). This increase in osmolarity will stimulate osmoreceptors in the hypothalamus which causes the secretion of ADH and also makes you thirsty. It's these measures that cause the reabsorption of water at the collecting duct and thus, increase mean arterial pressure. Remember, the biggest determinant of blood pressure is blood volume. This increase in blood volume will more than offset the increased GFR due to constriction of the efferent arteriole.

So, in my view, ADH is more involved with regulating plasma osmolarity while aldosterone is more involved with maining systemic pressure (by regulating body fluid volume). I haven't encountered any practice questions that challenged the way I think about these two hormones (yet) so this line of thinking has been working pretty well for me.
Hope this helps.
 
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rem6775

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Here's a previous post of mine regarding the differences between the ADH and RAAS systems:

The way I think about it, ADH secretion is primarily regulated by osmolarity. There are osmoreceptors in the hypothalamus that detect plasma osmolarity; if osmolarity increases, ADH secretion is stimulated (and you also become thirsty) so that you can reabsorb water to restore osmolarity.

I think of aldosterone more in the sense of body fluid volumes and systemic pressure. If you are hypotensive, the renin-angiotensin-aldosterone system (RAAS) is activated due to a decrease in GFR. This decrease in GFR stimulates renin secretion which ultimately leads to aldosterone secretion and Na+ reabsorption and thus, increases body fluid volume and pressure.

Aldosterone causes reabsorption of Na+ at the distal tubule but it has no direct effect on water reabsorption. What it does though is that it increases the blood osmolarity due to an increased reabsorption of Na+ (this reabsorption is NOT isosmotic). This increase in osmolarity will stimulate osmoreceptors in the hypothalamus which causes the secretion of ADH and also makes you thirsty. It's these measures that cause the reabsorption of water at the collecting duct and thus, increase mean arterial pressure. Remember, the biggest determinant of blood pressure is blood volume. This increase in blood volume will more than offset the increased GFR due to constriction of the efferent arteriole.

So, in my view, ADH is more involved with regulating plasma osmolarity while aldosterone is more involved with maining systemic pressure (by regulating body fluid volume). I haven't encountered any practice questions that challenged the way I think about these two hormones (yet) so this line of thinking has been working pretty well for me.
Hope this helps.
That statement is not true. And since when do you need to know any of this for the MCAT?

Aldosterone increases sodium absorption and water follows it. This is independent of any ADH action.
 

tncekm

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it seems pretty simple in my book, but the questions always seem to ask complicated stuff about ADH and aldosterone that i get wrong, and the relation of the kidney to all these things. can someone please clarify the kidneys role in
I'll try to answer at a level that I feel is sufficient for the MCAT :)

Blood pressure is regulated by the kidney PRIMARILY through the action of aldosterone.

Drops in blood pressure are sensed by the JGA, which is a structure found in EACH nephron and contains specialized cell groups called macula densa that are responsible for sensing the changes associated with drops in blood pressure. The macula densa will then tell the granulosa cells of the JGA to release "renin".

Renin is the initiator of the Renin-Angiotensin-Aldosterone System (RAAS).

Angiotensinogen --> Angiotensin I (via renin)
Angiotensin I --> Angiotensin II (via ACE, angiotensin converting enzyme)
Angiotensin II will then stimulate the production of Aldosterone in the zona glomerulosa layer of the adrenal gland.

Aldosterone will then go to work at the collecting ducts of the nephron by increasing sodium reabsorption from the tubular filtrate (the stuff inside the nephron / collecting duct that will be called urine later).

Sodium is the primary cation in the blood plasma, and is the major driviig force of blood volume as a result. E.g. blood osmolarity is 300 mOsm, and Na+ alone adcounts for nearly 145 mOsm. Just for kicks, it is accompanied by about 4-5 mOsm of K+, and those two cations (about 150 mOsm total) are balanced by 150 mOsm of anions, largely HCO3- (important for plasma buffering) and Cl-.

So, to recap, the JGA of the nephron picks up drops in blood pressure, stimulates renin release, which causes the RAA System to go into effect, which causes the blood volume to go up by virtue of the fact that it's pumping osmoles of Na+ into the blood.

ADH on the other hand "can" increase blood pressure, but it only does so when large volumes of blood are lost and it's primary function is to retrieve water from the collecting duct via increased expression of "aquaporin" proteins, which are water permeable. I know, I know... adding water should increase blood pressure via an increase in volume, right? Just memorize it... lol. These aquaporin receptors allow things to happen because the tubular fluid will lose water to the renal interstitum, which has a super high osmolarity (up to 1,200 mOsm under certain conditions).

Osmoreceptors in your hypothalamus will detect increases in osmolarity (which happens when water is lost) and stimulate production of ADH (aka vasopressin) in the hypothalamus, which is released inside the body of the neurohypophysis (the posterior pituitary).

Worth noting, that was not mentioned in your questions, is a hormone called ANP. This hormone responds to INCREASES in atrial pressure (the atria of your heart) and will essentially turn off the RAAS, specifically aldosterone.


So, to recap on ADH, ADH responds to decreases in osmolarity via osmoreceptors in the hypothalamus. It responds by increasing exprsesion of aquaporins in the collecting duct, which allows water to permeate the collecting duct and go into the medulla of the kidney, where the interstitial concentration can reach as high as 1,200 mOsm (drawing in the water).



I didn't check my work, so forgive me if there are problems and typos ^_^
 

tncekm

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That statement is not true. And since when do you need to know any of this for the MCAT?

Aldosterone increases sodium absorption and water follows it. This is independent of any ADH action.
Yeah, but that really is grey area. Aldosterone acts at the distal tubule / collecting duct, which is essentially impermeable to water without ADH increasing aquaporin expression. So, one could "argue" that aldosterone effects on water reabsorption are secondary to the effects of ADH. I think it's all semantic gobbledygook, but I don't think it matters that much anyway so long as people understand what is going on.
 
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dont overthink it. aldosterone increases (via renin/angiotensin) reabsorption of Na and excretion of K in the distal convoluted tubule. it acts to increase blood osmolarity (blood volume) and thus increases blood pressure. adh (vasopressin) just acts on the collecting duct to increase water reabsorption (think dehydration).

as a side note, calcium is reabsorbed in the distal convoluted tubule by pth and also increases blood osmolarity (pressure) but it will only be on the mcat in the context of bones.

thats at most all you need to know. even mentioning renin/angiotensin like i did above was overkill.
 

Charles_Carmichael

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That statement is not true. And since when do you need to know any of this for the MCAT?

Aldosterone increases sodium absorption and water follows it. This is independent of any ADH action.
Read what tncekm said. My statement was based on my understanding of the permeabilities of the different regions of the nephron. Water permeability of the prinicpal cells is regulated by ADH. With low ADH levels, there little to no water reabsorption. I don't think water can get through the tight epithelium present here without the help of aquaporins (controlled by ADH).
 

tncekm

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It's not covered in any detail, but they'll expect you to know basic stuff. Like, the job of the hypothalamus, pituitary, etc. EVERYTHING you need is covered in the MCAT prep books.
 

Ibn Alnafis MD

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Physio IS on the MCAT. It's not super complicated. Have you begun to study for it?
nope, I am planning to take it in spring of 2011. I have already taken all of the premed courses, and still don't know the detailed functions of organs. Do u recommend that I enroll in an anatomy/physiology course prior to taking the MCAT, or will the prep materials be sufficient?
 

illegallysmooth

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nope, I am planning to take it in spring of 2011. I have already taken all of the premed courses, and still don't know the detailed functions of organs. Do u recommend that I enroll in an anatomy/physiology course prior to taking the MCAT, or will the prep materials be sufficient?

The prep materials will be sufficient, I believe. If anything, the Kaplan course I took was a little over-enthusiastic about detailed physio.
 
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just think....if ur body has low bp it has means of increasing it through renin release. remeber about osmosis....solvents always want to move to an area with a higher concentration of solute....so when Aldo is released due to renin secretion....more Na+ goes into ur blood from ur urine therefore increasing BLOOD OSMOLARITY. once blood osmolarity is high....this will draw water out of your tissue increasing BP AND Blood Volume through ADH(Vasopressin) secretion from the hypothal. hope i explained this right from my understanding. good luck!
 
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quick note....ADH causes water retention...therefore after its effects....urine will be very concentrated (lots of solutes)
 

Charles_Carmichael

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just think....if ur body has low bp it has means of increasing it through renin release. remeber about osmosis....solvents always want to move to an area with a higher concentration of solute....so when Aldo is released due to renin secretion....more Na+ goes into ur blood from ur urine therefore increasing BLOOD OSMOLARITY. once blood osmolarity is high....this will draw water out of your tissue increasing BP AND Blood Volume through ADH(Vasopressin) secretion from the hypothal. hope i explained this right from my understanding. good luck!
Just a quick correction. The effects of aldosterone would end up resulting in increased water absorption from the kidneys. This would be the primary way to raise BP. I don't think the water drawn in from tissues (ie. ECF) would play a major role in increasing BP. Also, ADH is synthesized in the cell bodies of neurons (which are located in the hypothalamus) but it's actually secreted by the posterior pituitary.