PMID- 17206447
OWN - NLM
STAT- MEDLINE
DCOM- 20071024
LR  - 20181113
IS  - 0031-6768 (Print)
IS  - 0031-6768 (Linking)
VI  - 454
IP  - 1
DP  - 2007 Apr
TI  - Angiotensin type 1 (AT1) and type 2 (AT2) receptors mediate the increase in 
      TGF-beta1 in thyroid hormone-induced cardiac hypertrophy.
PG  - 75-81
AB  - Increased thyroid hormone (TH) levels are known to induce cardiac hypertrophy. 
      Some studies have provided evidence for a functional link between angiotensin II 
      (ANG II) and transforming growth factor beta1 (TGF-beta1) in the heart, both 
      being able to also induce cardiac hypertrophy. However, the contribution of this 
      growth factor activated directly by TH or indirectly by ANG II in cardiac 
      hypertrophy development remains unknown. To analyze the possible role of 
      TGF-beta1 in cardiac hypertrophy induced by TH and also to evaluate if the 
      TGF-beta1 effect is mediated by ANG II receptors, we employed Wistar rats 
      separated into control, hypothyroid (hypo) and hyperthyroid (T4 - 10) groups 
      combined or not with ANG II receptor blockers (losartan or PD123319). Serum 
      levels of T3 and T4, systolic pressure and heart rate confirmed the thyroid state 
      of the groups. The T4 - 10 group presented a significant increase in cardiac 
      TGF-beta1 levels; however, TGF-beta1 levels in the hypo group did not change in 
      relation to the control. Inhibition of the increase in cardiac TGF-beta1 levels 
      was observed in the groups treated with T4 in association with losartan or 
      PD123319 when compared to the T4 - 10 group. These results demonstrate for the 
      first time the TH-modulated induction of cardiac TGF-beta1 in cardiac 
      hypertrophy, and that this effect is mediated by ANG II receptors.
FAU - Diniz, G P
AU  - Diniz GP
AD  - Department of Anatomy, Institute of Biomedical Sciences, Universidade de Sao 
      Paulo, Avenida Prof. Lineu Prestes 2415, 05508-900 Sao Paulo, Brazil.
FAU - Carneiro-Ramos, M S
AU  - Carneiro-Ramos MS
FAU - Barreto-Chaves, M L M
AU  - Barreto-Chaves ML
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070106
PL  - Germany
TA  - Pflugers Arch
JT  - Pflugers Archiv : European journal of physiology
JID - 0154720
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Receptor, Angiotensin, Type 2)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 06LU7C9H1V (Triiodothyronine)
RN  - Q51BO43MG4 (Thyroxine)
SB  - IM
MH  - Animals
MH  - Blood Pressure
MH  - Cardiomegaly/*chemically induced/*metabolism/pathology/physiopathology
MH  - Heart Rate
MH  - Hyperthyroidism/chemically induced/complications/physiopathology
MH  - Hypothyroidism/complications/physiopathology
MH  - Myocardium/metabolism/pathology
MH  - Organ Size
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, Angiotensin, Type 1/*metabolism
MH  - Receptor, Angiotensin, Type 2/*metabolism
MH  - *Thyroxine/blood
MH  - Transforming Growth Factor beta1/genetics/*metabolism
MH  - Triiodothyronine/blood
EDAT- 2007/01/09 09:00
MHDA- 2007/10/25 09:00
CRDT- 2007/01/09 09:00
PHST- 2006/09/16 00:00 [received]
PHST- 2006/11/16 00:00 [accepted]
PHST- 2006/11/09 00:00 [revised]
PHST- 2007/01/09 09:00 [pubmed]
PHST- 2007/10/25 09:00 [medline]
PHST- 2007/01/09 09:00 [entrez]
AID - 10.1007/s00424-006-0192-0 [doi]
PST - ppublish
SO  - Pflugers Arch. 2007 Apr;454(1):75-81. doi: 10.1007/s00424-006-0192-0. Epub 2007 
      Jan 6.