PMID- 17072102
OWN - NLM
STAT- MEDLINE
DCOM- 20070104
LR  - 20190911
IS  - 1347-8613 (Print)
IS  - 1347-8613 (Linking)
VI  - 102
IP  - 3
DP  - 2006 Nov
TI  - Aldosterone synthesis and cytokine production in human peripheral blood 
      mononuclear cells.
PG  - 288-95
AB  - Previously, we reported that spironolactone reduced cytokine production in 
      cultured human peripheral blood mononuclear cells (PBMCs) with angiotensin (Ang) 
      II stimulation. To address the mechanisms underlying this effect, we examined the 
      contribution of aldosterone to cytokine production in cultured human PBMCs with 
      Ang II stimulation. PBMCs expressed the messenger RNA (mRNA) of Ang II type 1 
      receptor (AT1R) and mineralocorticoid receptor (MR) both spontaneously and after 
      Ang II stimulation, but expressed Ang II type 2 receptor (AT2R) under neither 
      condition. After 24 h of incubation, exogenous Ang II induced the expression of 
      CYP11B2 (a key enzyme of aldosterone synthesis) mRNA and caused aldosterone 
      synthesis. CV-11974 (an AT1R antagonist) reduced Ang II-induced aldosterone 
      synthesis, whereas PD-123319 (an AT2R antagonist) had no effect. The 
      concentration of aldosterone peaked earlier than those of monocyte 
      chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha). 
      After 48 h of incubation (under the influence of synthesized aldosterone), 
      CV-11974 and spironolactone significantly reduced the Ang II-enhanced production 
      of MCP-1 and TNF-alpha, whereas PD-123319 also had no effect. In conclusion, Ang 
      II induces aldosterone synthesis through AT1R and enhances cytokine production 
      through an AT1R-dependent mechanism and, at least partly, through a MR-dependent 
      mechanism in human PBMCs.
FAU - Miura, Ryuzea
AU  - Miura R
AD  - Department of Cardiovascular Medicine, Okayama University Graduate School of 
      Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. 
      miura@mpc.t.u-tokyo.ac.jp
FAU - Nakamura, Kazufumi
AU  - Nakamura K
FAU - Miura, Daiji
AU  - Miura D
FAU - Miura, Aya
AU  - Miura A
FAU - Hisamatsu, Kenichi
AU  - Hisamatsu K
FAU - Kajiya, Masahito
AU  - Kajiya M
FAU - Hashimoto, Katsushi
AU  - Hashimoto K
FAU - Nagase, Satoshi
AU  - Nagase S
FAU - Morita, Hiroshi
AU  - Morita H
FAU - Fukushima Kusano, Kengo
AU  - Fukushima Kusano K
FAU - Emori, Tetsuro
AU  - Emori T
FAU - Ishihara, Kazuhiko
AU  - Ishihara K
FAU - Ohe, Tohru
AU  - Ohe T
LA  - eng
PT  - Journal Article
DEP - 20061028
PL  - Japan
TA  - J Pharmacol Sci
JT  - Journal of pharmacological sciences
JID - 101167001
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (Angiotensin II Type 2 Receptor Blockers)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (DNA Primers)
RN  - 0 (Indicators and Reagents)
RN  - 0 (Mineralocorticoid Receptor Antagonists)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 11128-99-7 (Angiotensin II)
RN  - 4964P6T9RB (Aldosterone)
RN  - EC 1.14.15.4 (Cytochrome P-450 CYP11B2)
SB  - IM
MH  - Adult
MH  - Aldosterone/*biosynthesis
MH  - Angiotensin II/antagonists & inhibitors/pharmacology
MH  - Angiotensin II Type 1 Receptor Blockers/pharmacology
MH  - *Angiotensin II Type 2 Receptor Blockers
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis
MH  - Cytochrome P-450 CYP11B2/biosynthesis
MH  - Cytokines/*biosynthesis
MH  - DNA Primers/pharmacology
MH  - Female
MH  - Humans
MH  - Indicators and Reagents
MH  - Male
MH  - Mineralocorticoid Receptor Antagonists
MH  - Monocytes/drug effects/*metabolism
MH  - RNA, Messenger/biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Necrosis Factor-alpha/biosynthesis
EDAT- 2006/10/31 09:00
MHDA- 2007/01/05 09:00
CRDT- 2006/10/31 09:00
PHST- 2006/10/31 09:00 [pubmed]
PHST- 2007/01/05 09:00 [medline]
PHST- 2006/10/31 09:00 [entrez]
AID - JST.JSTAGE/jphs/FP0060801 [pii]
AID - 10.1254/jphs.fp0060801 [doi]
PST - ppublish
SO  - J Pharmacol Sci. 2006 Nov;102(3):288-95. doi: 10.1254/jphs.fp0060801. Epub 2006 
      Oct 28.