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Angiotensin II and renal arterioles

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Transformers

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Im confused...if there is Low blood pressure...triggering the RAAS system, why is it that in the EK passage, it says angiotensin II constricts the efferrent arteriole? I mean, this would increase GFR and thus increase urine output and decrease reabsorption to increase blood volume/pressure when an individual has low blood pressure.

I doubt that this is wrong, but ATII surely is not compensating for low blood pressure and I wanted to know why.
 

Omni

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One of the angiotensin makes a whole collage of things to happen. First of all, it is a vasoconstrictor. If you decrease the cross section of a tube, you will in turn increase the pressure. It also has the effect of causing the kidneys to release aldosterone, which causes more Na to be absorbed, and secondarily, water follows it. Hence, increasing the volume increases pressure. It also causes ADH release, which, as we know, causes retention of fluid.

Pretty much all these things serve to conserve blood pressure.
 

maverick09

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omni beat me to it. all i have to add is that the increased Na+ reabsorption increases cell osmolarity, thus stimulating thirst. fluid intake when the person drinks more water increases ECF volume and thus increases blood pressure
 

Charles_Carmichael

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One of the angiotensin makes a whole collage of things to happen. First of all, it is a vasoconstrictor. If you decrease the cross section of a tube, you will in turn increase the pressure. It also has the effect of causing the kidneys to release aldosterone, which causes more Na to be absorbed, and secondarily, water follows it. Hence, increasing the volume increases pressure. It also causes ADH release, which, as we know, causes retention of fluid.

Pretty much all these things serve to conserve blood pressure.
Just wanted to point out that it's the adrenal cortex that secretes aldosterone, not the kidneys. The kidneys secrete renin, which initiates the process of converting angiotensinogen to, ultimately, ATII. Other than that your post is spot on.

While ATII does increase GFR (by increasing upstream pressure at the glomerulus), you have to realize that there are other mechanisms that reabsorb more water.

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 MAP. 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.

Hope this helps.
 

drusillaaw

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Angiotensin II constricts the efferent arterioles in order to main adequate GFR, due to the the fact that the rest of the arteries are constricting due to lower bp (including the afferent arterioles). But like others said above, it is the other mechanisms of Angiotensin II (such as the stimulating aldosterone and Na+ reabsorption in the distal tublule, which leads to increased reabsorption of water) that counteract the decreased blood pressure.
 

Transformers

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it makes sense now; I mean I know that when BP changes by a little there are local regulatory mechanisms (autoregulation + tubuloglomerular feedback in which the macula densa secretes paracrines) so that GFR stays constant while BP changes slightly; but I guess this makes sense too with regard to AT IIs other affects...basically ATII sets up an increased GFR which is later counteracted by the reabsorption mechnasims by aldosterone and ADH...
 
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