PMID- 26290529
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150820
LR  - 20181113
IS  - 2051-817X (Print)
IS  - 2051-817X (Electronic)
IS  - 2051-817X (Linking)
VI  - 3
IP  - 8
DP  - 2015 Aug
TI  - Circulating angiotensin II deteriorates left ventricular function with 
      sympathoexcitation via brain angiotensin II receptor.
LID - 10.14814/phy2.12514 [doi]
LID - e12514
AB  - Sympathoexcitation contributes to the progression of heart failure. Activation of 
      brain angiotensin II type 1 receptors (AT1R) causes central sympathoexcitation. 
      Thus, we assessed the hypothesis that the increase in circulating angiotensin II 
      comparable to that reported in heart failure model affects cardiac function 
      through the central sympathoexcitation via activating AT1R in the brain. In 
      Sprague-Dawley rats, the subcutaneous infusion of angiotensin II for 14 days 
      increased the circulating angiotensin II level comparable to that reported in 
      heart failure model rats after myocardial infarction. In comparison with the 
      control, angiotensin II infusion increased 24 hours urinary norepinephrine 
      excretion, and systolic blood pressure. Angiotensin II infusion hypertrophied 
      left ventricular (LV) without changing chamber dimensions while increased 
      end-diastolic pressure. The LV pressure -: volume relationship indicated that 
      angiotensin II did not impact on the end-systolic elastance, whereas 
      significantly increased end-diastolic elastance. Chronic intracerebroventricular 
      infusion of AT1R blocker, losartan, attenuated these angiotensin II-induced 
      changes. In conclusion, circulating angiotensin II in heart failure is capable of 
      inducing sympathoexcitation via in part AT1R in the brain, subsequently leading 
      to LV diastolic dysfunction.
CI  - (c) 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on 
      behalf of the American Physiological Society and The Physiological Society.
FAU - Shinohara, Keisuke
AU  - Shinohara K
AD  - Departments of Cardiovascular Medicine, Kyushu University Graduate School of 
      Medical Sciences, Fukuoka, Japan.
FAU - Kishi, Takuya
AU  - Kishi T
AD  - Department of Advanced Therapeutics for Cardiovascular Diseases, Kyushu 
      University Graduate School of Medical Sciences, Fukuoka, Japan 
      tkishi@cardiol.med.kyushu-u.ac.jp.
FAU - Hirooka, Yoshitaka
AU  - Hirooka Y
AD  - Department of Cardiovascular Regulation and Therapeutics, Kyushu University 
      Graduate School of Medical Sciences, Fukuoka, Japan.
FAU - Sunagawa, Kenji
AU  - Sunagawa K
AD  - Departments of Cardiovascular Medicine, Kyushu University Graduate School of 
      Medical Sciences, Fukuoka, Japan.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Physiol Rep
JT  - Physiological reports
JID - 101607800
PMC - PMC4562594
OTO - NOTNLM
OT  - Angiotensin II
OT  - heart failure
OT  - sympathetic nerve activity
EDAT- 2015/08/21 06:00
MHDA- 2015/08/21 06:01
PMCR- 2015/08/19
CRDT- 2015/08/21 06:00
PHST- 2015/08/21 06:00 [entrez]
PHST- 2015/08/21 06:00 [pubmed]
PHST- 2015/08/21 06:01 [medline]
PHST- 2015/08/19 00:00 [pmc-release]
AID - 3/8/e12514 [pii]
AID - 10.14814/phy2.12514 [doi]
PST - ppublish
SO  - Physiol Rep. 2015 Aug;3(8):e12514. doi: 10.14814/phy2.12514.