anatomy Forum Guru
Topics: 101 Posts: 423
| | 11/10/04 - 05:16 PM  
 
   
 
|   #1 |
In def of 17 alpha-hydroxylase why there is increase in the production of 11-deoxycorticosterone and corticosterone? as we know it that this enzyme effects only adrenal zona fasciculata and zona reticularis.there is no any role of these in this those r concernd with zona glomerulosa. according to kaplan physio they said that they both inc b/c of ACTH. CAN ANY ONE OF U UNDERSTAND MY POINT OR NOT. :roll: PLS REPLY THANX
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| vrach Forum Junior
Topics: 3 Posts: 79
| | 11/11/04 - 06:19 AM  
 
   
 
|   #2 |
If you look at the diagram for the hormone synthesis pathway in Kaplan for the zona fasiculate, you ahould notice that both deoxycorticosterone and cortisone are also synthesized in this region. They are not converted to aldosterone, since the zona fasiculata does not have the enzyme Aldosterone synthetase. In 17 hydroxylase deficiency, the lack of cortisol and its negative feedback, leads to elevated ACTH and hypertrophy of the zona fasiculata and reticularis. At this point the only working enzyme pathway in the zona fasiculata leads to the excessive synthesis of deoxycorticosterone and corticosterone.
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| mjl1717 Forum Hero

Topics: 957 Posts: 5,461
| | 11/11/04 - 09:56 AM  
 
   
 
|   #3 |
Ill try to explain this in less then 10 steps: 1)corticosterone is made in the glomerulosa,cortisol in the z. fasciculata androstenedione is made in the z. reticularis/ but in reality I think the last 2 substrates are both made in the z.fasciculata and z. reticularis 2)This is how I see it(due to the bodies"infinite wisedom" In 17 hydroxylase deficiency cortisol and androstenedione are BLOCKED or KNOCKED OUT! 3)No cortisol,No androgen*** -ACTH is very much ACTIVE 4)Im still in the adrenal cortex/This excess. ACTH cause adrenal hyperplasia and increase steroids before the block in the z. glomerulosa. Im talking about deoxycorticosterone and corticosterone{forget about pregnenolone and progesterone. 5)The infinite wisedom of the body is that deoxycorticosterone is also weak mineralcorticoid and corticosterone is a weak glucocorticoid. 6)**Excess ACTH stimulates the above 2 and you get Na retension and increase BP{This is in the z. glomerulosa. 7)The increase B.P. decreases renin, angiotensinII and aldosterone 8)Ultimately aldostrone is decreased and the z.glomerulosa is shut down. *By the way ACTH DOES have minor importance in aldosterone secretion but physiologically stimulation of aldosterone is under the renin angiotensin system and increase K. Hope this helps :shock:
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| anatomy Forum Guru
Topics: 101 Posts: 423
| | 11/11/04 - 12:46 PM  
 
   
 
|   #4 |
thanx alot for nice reply. good luck
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