PMID- 27822383
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211103
IS  - 2056-5909 (Print)
IS  - 2056-5909 (Electronic)
IS  - 2056-5909 (Linking)
VI  - 22
DP  - 2016
TI  - Neuronal nitric oxide synthase in hypertension - an update.
PG  - 20
LID - 20
AB  - Hypertension is a prevalent condition worldwide and is the key risk factor for 
      fatal cardiovascular complications, such as stroke, sudden cardiac death and 
      heart failure. Reduced bioavailability of nitric oxide (NO) in the endothelium is 
      an important precursor for impaired vasodilation and hypertension. In the heart, 
      NO deficiency deteriorates the adverse consequences of pressure-overload and 
      causes cardiac hypertrophy, fibrosis and myocardial infarction which lead to 
      fatal heart failure and sudden cardiac death. Recent consensus is that both 
      endothelial and neuronal nitric oxide synthases (eNOS or NOS3 and nNOS or NOS1) 
      are the constitutive sources of NO in the myocardium. Between the two, nNOS is 
      the predominant isoform of NOS that controls intracellular Ca(2+) homeostasis, 
      myocyte contraction, relaxation and signaling pathways including nitroso-redox 
      balance. Notably, our recent research indicates that cardiac eNOS protein is 
      reduced but nNOS protein expression and activity are increased in hypertension. 
      Furthermore, nNOS is induced by the interplay between angiotensin II (Ang II) 
      type 1 receptor (AT1R) and Ang II type 2 receptor (AT2R), mediated by NADPH 
      oxidase and reactive oxygen species (ROS)-dependent eNOS activity in cardiac 
      myocytes. nNOS, in turn, protects the heart from pathogenesis via positive 
      lusitropy in hypertension. Soluble guanylate cyclase (sGC)-cGMP/PKG-dependent 
      phosphorylation of myofilament proteins are novel targets of nNOS in hypertensive 
      myocardium. In this short review, we will endeavor to overview new findings 
      of the up-stream and downstream regulation of cardiac nNOS in hypertension, shed 
      light on the underlying mechanisms which may be of therapeutic value in 
      hypertensive cardiomyopathy.
FAU - Zhang, Yin Hua
AU  - Zhang YH
AD  - Department of Physiology & Biomedical Sciences, Ischemic/Hypoxic Disease 
      Institute, Seoul National University, College of Medicine, 103 Dae Hak Ro, Chong 
      No Gu, 110-799 Seoul Korea ; Yanbian University Hospital, Yanji, Jilin Province 
      133000 China ; Division of Cardiovascular Sciences, School of Medical Sciences, 
      Faculty of Biology, Medicine and Health, University of Manchester, Manchester, 
      UK.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20161103
PL  - England
TA  - Clin Hypertens
JT  - Clinical hypertension
JID - 101669508
PMC - PMC5093926
OTO - NOTNLM
OT  - Cardiomyocyte
OT  - Hypertension
OT  - Hypertrophy
OT  - Neuronal nitric oxide synthase (nNOS)
OT  - Nitric oxide
EDAT- 2016/11/09 06:00
MHDA- 2016/11/09 06:01
PMCR- 2016/11/03
CRDT- 2016/11/09 06:00
PHST- 2016/07/15 00:00 [received]
PHST- 2016/10/19 00:00 [accepted]
PHST- 2016/11/09 06:00 [entrez]
PHST- 2016/11/09 06:00 [pubmed]
PHST- 2016/11/09 06:01 [medline]
PHST- 2016/11/03 00:00 [pmc-release]
AID - 55 [pii]
AID - 10.1186/s40885-016-0055-8 [doi]
PST - epublish
SO  - Clin Hypertens. 2016 Nov 3;22:20. doi: 10.1186/s40885-016-0055-8. eCollection 
      2016.