PMID- 23235923
OWN - NLM
STAT- MEDLINE
DCOM- 20130903
LR  - 20141120
IS  - 1439-4286 (Electronic)
IS  - 0018-5043 (Linking)
VI  - 45
IP  - 2
DP  - 2013 Feb
TI  - Control of CYP11B2/CYP11B1 expression ratio and consequences for the zonation of 
      the adrenal cortex.
PG  - 81-5
LID - 10.1055/s-0032-1331210 [doi]
AB  - Access of corticotropin to glucocorticoid synthesis in adrenocortical cells is 
      provided by the expression of the ACTH receptor (MC2R). Activation of the MC2R 
      increases stimulatory G-protein, adenylyl cyclase, and protein kinase A (PKA) 
      activities. Furthermore, PKA phosphorylates transcription factors that have a 
      stimulating effect on glucocorticoid synthesis. Sensitivity of adrenocortical 
      cells to renin/angiotensin-2 is conferred by the expression of the inhibitory 
      G-protein-linked angiotensin-2 type 1 receptor (AT1R) that additionally 
      associates to the phospholipase C-activating G-protein q. The AT1R is connected 
      to the adrenal potassium sensory system and regulates calcium influx as well as 
      phospholipase C-beta (PLC-beta) and thus calmodulin kinase-dependent transcription of 
      steroidogenic enzymes. While AT1R signaling suppresses the influence of 
      corticotropin on the generation of cyclic adenosine monophosphate, the expression 
      of the AT1R and its associated enzyme activities are under the control of 
      glucocorticoids. Thus, dominance of one of the two signaling pathways is 
      dependent on two factors: the extracellular concentration of their ligands and 
      the products of their signaling pathways. These findings are in favor of the 
      hypothesis that the centripetal blood flow through the adrenal gland builds up a 
      glucocorticoid gradient creating a morphogenetic field along which adrenal 
      cortical cells adopt different functional states, leading to the typical zonation 
      of the adrenal cortex.
CI  - (c) Georg Thieme Verlag KG Stuttgart . New York.
FAU - Dringenberg, T
AU  - Dringenberg T
AD  - Department of Endocrinology, Diabetes and Metabolism, Medical Faculty, University 
      of Dusseldorf, Dusseldorf, Germany.
FAU - Schwitalla, M
AU  - Schwitalla M
FAU - Haase, M
AU  - Haase M
FAU - Scherbaum, W A
AU  - Scherbaum WA
FAU - Willenberg, H S
AU  - Willenberg HS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121212
PL  - Germany
TA  - Horm Metab Res
JT  - Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et 
      metabolisme
JID - 0177722
RN  - 0 (Adrenal Cortex Hormones)
RN  - 0 (Receptors, Corticotropin)
RN  - 0 (Steroidogenic Factor 1)
RN  - EC 1.14.15.4 (Cytochrome P-450 CYP11B2)
RN  - EC 1.14.15.4 (Steroid 11-beta-Hydroxylase)
SB  - IM
MH  - Adrenal Cortex/blood supply/*enzymology/metabolism
MH  - Adrenal Cortex Hormones/genetics/metabolism
MH  - Animals
MH  - Cytochrome P-450 CYP11B2/genetics/*metabolism
MH  - *Gene Expression Regulation, Enzymologic
MH  - Humans
MH  - Receptors, Corticotropin/genetics/metabolism
MH  - Signal Transduction
MH  - Steroid 11-beta-Hydroxylase/genetics/*metabolism
MH  - Steroidogenic Factor 1/genetics/metabolism
EDAT- 2012/12/14 06:00
MHDA- 2013/09/04 06:00
CRDT- 2012/12/14 06:00
PHST- 2012/12/14 06:00 [entrez]
PHST- 2012/12/14 06:00 [pubmed]
PHST- 2013/09/04 06:00 [medline]
AID - 10.1055/s-0032-1331210 [doi]
PST - ppublish
SO  - Horm Metab Res. 2013 Feb;45(2):81-5. doi: 10.1055/s-0032-1331210. Epub 2012 Dec 
      12.