PMID- 27417104
OWN - NLM
STAT- MEDLINE
DCOM- 20170629
LR  - 20220409
IS  - 1432-2013 (Electronic)
IS  - 0031-6768 (Linking)
VI  - 468
IP  - 9
DP  - 2016 Sep
TI  - Hyperhomocysteinemia impairs regional blood flow: involvements of endothelial and 
      neuronal nitric oxide.
PG  - 1517-25
LID - 10.1007/s00424-016-1849-y [doi]
AB  - Increasing evidence support the idea that hyperhomocysteinemia (HHcy) is 
      responsible for pathogenesis underlying cerebral, coronary, renal, and other 
      vascular circulatory disorders and for hypertension. Impaired synthesis of nitric 
      oxide (NO) in the endothelium or increased production of asymmetric 
      dimethylarginine and activated oxygen species are involved in the impairment of 
      vasodilator effects of NO. Impaired circulation in the brain derived from reduced 
      synthesis and actions of NO would be an important triggering factor to dementia 
      and Alzheimer's disease. Reduced actions of NO and brain hypoperfusion trigger 
      increased production of amyloid-beta that inhibits endothelial function, thus 
      establishing a vicious cycle for impairing brain circulation. HHcy is involved in 
      the genesis of anginal attack and coronary myocardial infarction. HHcy is also 
      involved in renal circulatory diseases. The homocysteine (Hcy)-induced 
      circulatory failure is promoted by methionine and is prevented by increased folic 
      acid and vitamin B6/B12. Eliminating poor life styles, such as smoking and being 
      sedentary; keeping favorable dietary habits; and early treatment maintaining 
      constitutive NOS functions healthy, reducing oxidative stresses would be 
      beneficial in protecting HHcy-induced circulatory failures.
FAU - Toda, Noboru
AU  - Toda N
AUID- ORCID: 0000-0003-4035-7365
AD  - Toyama Institute for Cardiovascular Pharmacology Research, 7-13, 1-Chome, 
      Azuchimachi, Chuo-ku, Osaka, 541-0052, Japan. n.toda.toyama-bldg@orion.ocn.ne.jp.
FAU - Okamura, Tomio
AU  - Okamura T
AD  - Department of Pharmacology, Shiga University of Medical Science, Seta, Otsu, 
      Shiga, 520-2192, Japan.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20160714
PL  - Germany
TA  - Pflugers Arch
JT  - Pflugers Archiv : European journal of physiology
JID - 0154720
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type I)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
SB  - IM
MH  - Animals
MH  - *Cerebrovascular Circulation
MH  - *Coronary Circulation
MH  - Humans
MH  - Hyperhomocysteinemia/enzymology/*metabolism/physiopathology
MH  - Nitric Oxide Synthase Type I/*metabolism
MH  - Nitric Oxide Synthase Type III/*metabolism
OTO - NOTNLM
OT  - Cerebral blood flow
OT  - Coronary blood flow
OT  - Hyperhomocysteinemia
OT  - Nitric oxide
OT  - Oxidative stress
EDAT- 2016/07/16 06:00
MHDA- 2017/07/01 06:00
CRDT- 2016/07/16 06:00
PHST- 2016/04/12 00:00 [received]
PHST- 2016/06/08 00:00 [accepted]
PHST- 2016/06/06 00:00 [revised]
PHST- 2016/07/16 06:00 [entrez]
PHST- 2016/07/16 06:00 [pubmed]
PHST- 2017/07/01 06:00 [medline]
AID - 10.1007/s00424-016-1849-y [pii]
AID - 10.1007/s00424-016-1849-y [doi]
PST - ppublish
SO  - Pflugers Arch. 2016 Sep;468(9):1517-25. doi: 10.1007/s00424-016-1849-y. Epub 2016 
      Jul 14.