Please Help: The urinary system: Mineralocorticoids and Glucocorticoids,

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science squad
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#1
Report Thread starter 3 years ago
#1
Hi,
I was hoping that someone could possibly help me to understand the following question in my latest Biology assignment:

"How do abnormal concentrations of mineralocorticoids e.g. aldosterone, and glucocorticoids, affect urine formation?

I've been researching for a while now and the only information that i've been able to find, is how a deficiency in Aldosterone and Cortisol can result from Addison’s disease which is an adrenal gland issue but nothing is ever stated about that composition of the urine it produces?

Any help would be greatly appreciated
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*ash
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#2
Report 3 years ago
#2
I have found from a source that cortisol decreases ADH levels. ADH is a peptide hormone required for water reabsorption into blood at the collecting tubules in kidneys. So in high cortisol levels, less ADH is secreted from posterior pituitary gland and so less water is reabsorbed from urine so urine is more dilute.

Aldosterone increases Na+ reabsorption in the collecting tubules, in the absence of ADH the collecting duct is impermeable to water so water reabsorption into blood via osmosis will not take place. This means the urine will be more dilute.

HOWEVER please not that high aldosterone levels does not necessarily correlate with dilute urine because in the presence of ADH it actually increases water reabsorption as part of a system known as renin-angiotensin-aldosterone system (RAAS).

Sources:
http://www.adrenaladvice.com/adrenal...rination.shtml [Accessed 31/05/2018].
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macpatgh-Sheldon
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#3
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#3
Hi,

As mentioned by *ash above, the renin-angiotensin-aldosterone axis as it is called, helps maintain the sodium levels in the blood and ultimately in the body. The reabsorption of Na+ ions in the proximal tubule cells is an active transport process achieved via the Na+, K+ - ATPase mechanism [also called the sodium/potassium pump]. Three Na+ ions are reabsorbed in exchange for 2 K+ ions being excreted.

Na+ has several crucial roles in the body, not least the maintenance of the osmolality (low water potential) of the blood so that it aids reabsorption of water in the collecting ducts of the kidney - it is also important to note that Na+ is predominantly an extracellular ion, whereas K+ is mainly intracellular [normal serum Na+ level = 135-150 mmoles/l; K+ level = 3.5-5.1 mmoles/l [at least at the hospital I trained at - varies slightly between labs]]. One other role of Na+ is the creation of the resting potential of neurones [-70mV inside the cell].

If you work it out, in Addison's disease, in which there is underactivity of the adrenal cortex (outer layer of adrenal glands)[also called supra-renal glands as they are located like caps above the kidneys] the patient will suffer from low Na+ in the blood which reduces blood volume, thereby reducing venous return to the heart and by the Frank-Starling Law, this reduces stroke volume and hence blood pressure. Actually, some patients with Addison's can have life-threateningly low blood pressure, and possible collapse. The sodium is lost in exchange for K+ so K+ is retained causing hyperkalemia (high K+ in blood) and this can cause bradyarrhythmias (slow, irregular heart rhythm).

Conversely, in Conn's syndrome (oversecretion of mineralocorticoids from the adrenal cortex, the patient retains Na+ [and therefore water by osmosis] so will have hypertension, but also hypokalaemia [low K+] as K+ has been lost in exchange for Na+. Low K+ can lead to serious cardiac tachyarrhythmias [fast irregular heart rhythm].

One effect of glucocorticoids e.g, cortisol on kidney function is due to the anti-insulin action of these steroids. They tend to reverse the hypoglycaemic [glucose lowering] action of insulin, causing relative hyperglycaemia [high blood glucose] by several mechanisms which are mostly the opposite of the actions of insulin e.g. steroids tend to increase glycogenolysis [breakdown of glycogen into glucose] and gluconeogenesis (Greek neo = new; genesis = creation as in Bible! therefore production of new glucose mainly from proteins). Therefore, one problem in patients with Cushing's syndrome is secondary diabetes mellitus, AND THIS CAN LEAD TO GLYCOSURIA (glucose in the urine due to blood levels exceeding the renal threshold = 180 mg/100ml). Glucose in urine reduces water potential of urine drawing water into the urine compartment [from blood] so the patient suffers polyuria [passing too much water, which is a common presenting symptom also of primary diabetes], and hence polydipsia [increased thirst].

Look up ALL the new words you pick up from my post, and you will start off a good essay!

Best of luck!

M
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science squad
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#4
Report Thread starter 3 years ago
#4
Thank you both very much for your excellent explanations, because of you, i've now finally managed to finish the question.
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macpatgh-Sheldon
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#5
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#5
(Original post by science squad)
Thank you both very much for your excellent explanations, because of you, i've now finally managed to finish the question.
Pleased for you
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