PMID- 16156509
OWN - NLM
STAT- MEDLINE
DCOM- 20051005
LR  - 20170922
IS  - 0916-9636 (Print)
IS  - 0916-9636 (Linking)
VI  - 28
IP  - 5
DP  - 2005 May
TI  - Excess aldosterone under normal salt diet induces cardiac hypertrophy and 
      infiltration via oxidative stress.
PG  - 447-55
AB  - Aldosterone is known to play a role in the pathophysiology of some cardiovascular 
      diseases. However, previous studies on aldosterone infusion have been mostly 
      performed in animals receiving sodium loading and uninephrectomy, and thus the 
      cardiac action of aldosterone alone remains to be fully clarified. The present 
      study was undertaken to investigate the direct cardiac action of aldosterone 
      infusion alone in rats not subjected to salt loading and uninephrectomy. 
      Aldosterone (0.75 microg/h) was subcutaneously infused into rats via an osmotic 
      minipump for 14 days. Aldosterone infusion, under a normal salt diet, induced 
      only a slight increase in the blood pressure of normal rats throughout the 
      infusion. However, aldosterone significantly induced cardiac hypertrophy, as 
      shown by echocardiography and measurement of cardiomyocyte cross-sectional area. 
      Furthermore, aldosterone caused not only cardiac interstitial macrophage 
      infiltration but also cardiac focal inflammatory lesions, which were associated 
      with an increase in cardiac monocyte chemoattractant protein-1 (MCP-1) and 
      osteopontin mRNA. The slight elevation of blood pressure by aldosterone infusion 
      was completely prevented by tempol, the superoxide dismutase mimetic. However, 
      tempol failed to suppress cardiac hypertrophy, the formation of inflammatory 
      lesions, and upregulation of cardiac MCP-1 and osteopontin by aldosterone, while 
      N-acetylcysteine could inhibit all of them. Our data provide evidence that 
      aldosterone alone can induce cardiac hypertrophy and severe inflammatory response 
      in the heart, independently of blood pressure, even in the absence of salt 
      loading or nephrectomy. Aldosterone seems to induce cardiac inflammation and gene 
      expression via oxidative stress that is inhibited by N-acetylcysteine but not by 
      tempol.
FAU - Yoshida, Kaoru
AU  - Yoshida K
AD  - Department of Pharmacology, Osaka City University Graduate School of Medical 
      Science, Osaka, Japan.
FAU - Kim-Mitsuyama, Shokei
AU  - Kim-Mitsuyama S
FAU - Wake, Ryotaro
AU  - Wake R
FAU - Izumiya, Yasuhiro
AU  - Izumiya Y
FAU - Izumi, Yasukatsu
AU  - Izumi Y
FAU - Yukimura, Tokihito
AU  - Yukimura T
FAU - Ueda, Makiko
AU  - Ueda M
FAU - Yoshiyama, Minoru
AU  - Yoshiyama M
FAU - Iwao, Hiroshi
AU  - Iwao H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Hypertens Res
JT  - Hypertension research : official journal of the Japanese Society of Hypertension
JID - 9307690
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Sialoglycoproteins)
RN  - 0 (Sodium Chloride, Dietary)
RN  - 0 (Spp1 protein, rat)
RN  - 106441-73-0 (Osteopontin)
RN  - 4964P6T9RB (Aldosterone)
RN  - WYQ7N0BPYC (Acetylcysteine)
SB  - IM
EIN - Hypertens Res. 2016 Jun;39(6):482. PMID: 27264876
MH  - Acetylcysteine/pharmacology
MH  - Aldosterone/blood/pharmacology
MH  - Animals
MH  - Blood Pressure/drug effects
MH  - Cardiomegaly/diagnostic imaging/*etiology/*metabolism
MH  - Chemokine CCL2/genetics
MH  - Echocardiography
MH  - Hyperaldosteronism/chemically induced/*complications/*metabolism
MH  - Male
MH  - Myocarditis/diagnostic imaging/etiology/metabolism
MH  - Osteopontin
MH  - *Oxidative Stress
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sialoglycoproteins/genetics
MH  - Sodium Chloride, Dietary/pharmacology
EDAT- 2005/09/15 09:00
MHDA- 2005/10/06 09:00
CRDT- 2005/09/15 09:00
PHST- 2005/09/15 09:00 [pubmed]
PHST- 2005/10/06 09:00 [medline]
PHST- 2005/09/15 09:00 [entrez]
AID - 10.1291/hypres.28.447 [doi]
PST - ppublish
SO  - Hypertens Res. 2005 May;28(5):447-55. doi: 10.1291/hypres.28.447.