PMID- 18716362
OWN - NLM
STAT- MEDLINE
DCOM- 20080909
LR  - 20220311
IS  - 0916-9636 (Print)
IS  - 0916-9636 (Linking)
VI  - 31
IP  - 6
DP  - 2008 Jun
TI  - Combination therapy with renin-angiotensin system inhibitors and the calcium 
      channel blocker azelnidipine decreases plasma inflammatory markers and urinary 
      oxidative stress markers in patients with diabetic nephropathy.
PG  - 1147-55
LID - 10.1291/hypres.31.1147 [doi]
AB  - A calcium channel blocker (CCB), azelnidipine (AZ), is reported to inhibit 
      oxidative stresses, particularly when administered under blockade of the 
      renin-angiotensin system (RAS). The purpose of this study was to investigate 
      whether AZ inhibits oxidative stresses more potently than other CCBs under 
      blockade of RAS and exerts renoprotection in type 2 diabetic nephropathy. 
      Subjects were hypertensive type 2 diabetics with nephropathy, taking RAS 
      inhibitors. The patients were randomly assigned to two groups, an AZ group (n=21, 
      16 mg/d) and a nifedipine-CR (NF) group (n=17, 40 mg/d). The plasma levels of 
      monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), high-sensitive 
      C-reactive protein (hsCRP), adiponectin and tumor necrosis factor-alpha 
      (TNF(alpha)), the urinary excretion of 8-epi-prostaglandin F(2alpha) 
      (8-epi-PGF(2alpha)) and 8-hydroxydeoxyguanosine (8-OHdG), and the urinary 
      albumin-to-creatinine ratios (ACR) were determined before and after 16-week 
      treatment. Neither metabolic parameters nor blood pressure levels differed 
      between the two groups not only at baseline but also after the treatment. 
      However, significant decreases in MCP-1, IL-6, hsCRP, TNF(alpha), 
      8-epi-PGF(2alpha), 8-OHdG and ACR levels, and a significant increase in the 
      plasma adiponectin level were detected in the AZ group, but not in the NF group. 
      The % change in the urinary oxidative stress markers correlated with that in ACR. 
      Our results indicate that, in hypertensive patients with diabetic nephropathy, a 
      combination therapy of RAS inhibitors and AZ is an effective therapeutic modality 
      for decreasing not only blood pressure but also inflammations and oxidative 
      stresses.
FAU - Ogawa, Susumu
AU  - Ogawa S
AD  - Division of Nephrology, Endocrinology and Vascular Medicine, Tohoku University 
      Hospital, Aoba-ku, Sendai, Japan. ogawa-s@mail.tains.tohoku.ac.jp
FAU - Mori, Takefumi
AU  - Mori T
FAU - Nako, Kazuhiro
AU  - Nako K
FAU - Ito, Sadayoshi
AU  - Ito S
LA  - eng
PT  - Journal Article
PT  - Randomized Controlled Trial
PL  - England
TA  - Hypertens Res
JT  - Hypertension research : official journal of the Japanese Society of Hypertension
JID - 9307690
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Dihydropyridines)
RN  - 0 (Interleukin-6)
RN  - 27415-26-5 (8-epi-prostaglandin F2alpha)
RN  - 5GZ3E0L9ZU (Azetidinecarboxylic Acid)
RN  - 88847-89-6 (8-Hydroxy-2'-Deoxyguanosine)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - AYI8EX34EU (Creatinine)
RN  - B7IN85G1HY (Dinoprost)
RN  - G9481N71RO (Deoxyguanosine)
RN  - PV23P19YUG (azelnidipine)
SB  - IM
MH  - 8-Hydroxy-2'-Deoxyguanosine
MH  - Adult
MH  - Aged
MH  - Angiotensin II Type 1 Receptor Blockers/*administration & dosage
MH  - Angiotensin-Converting Enzyme Inhibitors/*administration & dosage
MH  - Azetidinecarboxylic Acid/administration & dosage/*analogs & derivatives
MH  - C-Reactive Protein/analysis
MH  - Calcium Channel Blockers/*administration & dosage
MH  - Creatinine/urine
MH  - Deoxyguanosine/analogs & derivatives/urine
MH  - Diabetic Nephropathies/*drug therapy/metabolism
MH  - Dihydropyridines/*administration & dosage
MH  - Dinoprost/analogs & derivatives/urine
MH  - Drug Therapy, Combination
MH  - Female
MH  - Humans
MH  - Interleukin-6/blood
MH  - Male
MH  - Middle Aged
MH  - *Oxidative Stress
EDAT- 2008/08/22 09:00
MHDA- 2008/09/10 09:00
CRDT- 2008/08/22 09:00
PHST- 2008/08/22 09:00 [pubmed]
PHST- 2008/09/10 09:00 [medline]
PHST- 2008/08/22 09:00 [entrez]
AID - JST.JSTAGE/hypres/31.1147 [pii]
AID - 10.1291/hypres.31.1147 [doi]
PST - ppublish
SO  - Hypertens Res. 2008 Jun;31(6):1147-55. doi: 10.1291/hypres.31.1147.