PMID- 23736684
OWN - NLM
STAT- MEDLINE
DCOM- 20140218
LR  - 20130724
IS  - 1423-0313 (Electronic)
IS  - 0031-7012 (Linking)
VI  - 91
IP  - 5-6
DP  - 2013
TI  - Attenuation of conducted vasodilation in skeletal muscle arterioles during 
      hyperhomocysteinemia.
PG  - 287-96
LID - 10.1159/000350394 [doi]
AB  - BACKGROUND: Vasomotor responses conducted from terminal arterioles to proximal 
      vessels may contribute to match tissue demands and blood supply during skeletal 
      muscle contraction. Conduction of vasodilatation (CVD) from distal resistance 
      arterioles to the proximal arterioles and feeding arteries during metabolic 
      demand is mediated by intercellular gap junctions in the vascular endothelium. 
      The role of hyperhomocysteinemia (HHcy) in the musculoskeletal system during CVD 
      is unclear. We hypothesize that during HHcy, there is impaired CVD due to 
      decreased expression of endothelial-associated connexins and thus decreased 
      tissue perfusion to the contracting skeletal muscles. METHODS: CVD studies were 
      performed in a gluteus maximus muscle preparation of wild-type (C57BL6/J) and 
      CBS-/+ (HHcy) mice using intravital microscopy. Expression of connexins and 
      myostatin protein (an antiskeletal muscle statin) was studied by Western blot and 
      immunohistochemistry methods. Tissue perfusion to acetylcholine was assessed by 
      the laser Doppler technique. RESULTS: There was decreased CVD and tissue 
      perfusion in response to acetylcholine in CBS-/+ mice compared to wild-type 
      controls. There was decreased expression of connexins 37, 40 and 43 and increased 
      expression of myostatin in CBS-/+ mice compared to wild-type controls. 
      CONCLUSION: Our findings suggest that CVD in skeletal muscle is decreased during 
      HHcy due to decreased expression of gap junction connexins.
CI  - Copyright (c) 2013 S. Karger AG, Basel.
FAU - Givvimani, S
AU  - Givvimani S
AD  - Department of Physiology and Biophysics, University of Louisville School of 
      Medicine, Louisville, Ky., USA. s0givv01@louisville.edu
FAU - Narayanan, N
AU  - Narayanan N
FAU - Armaghan, F
AU  - Armaghan F
FAU - Pushpakumar, S
AU  - Pushpakumar S
FAU - Tyagi, S C
AU  - Tyagi SC
LA  - eng
GR  - HL-108621/HL/NHLBI NIH HHS/United States
GR  - HL-74185/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20130601
PL  - Switzerland
TA  - Pharmacology
JT  - Pharmacology
JID - 0152016
RN  - 0 (Connexins)
RN  - 0 (Mstn protein, mouse)
RN  - 0 (Myostatin)
RN  - 9007-34-5 (Collagen)
SB  - IM
MH  - Animals
MH  - Arterioles/*physiopathology
MH  - Collagen/metabolism
MH  - Connexins/metabolism
MH  - Hyperhomocysteinemia/metabolism/*physiopathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Muscle, Skeletal/*blood supply/metabolism
MH  - Myostatin/metabolism
MH  - Vasodilation
EDAT- 2013/06/06 06:00
MHDA- 2014/02/19 06:00
CRDT- 2013/06/06 06:00
PHST- 2013/01/10 00:00 [received]
PHST- 2013/03/03 00:00 [accepted]
PHST- 2013/06/06 06:00 [entrez]
PHST- 2013/06/06 06:00 [pubmed]
PHST- 2014/02/19 06:00 [medline]
AID - 000350394 [pii]
AID - 10.1159/000350394 [doi]
PST - ppublish
SO  - Pharmacology. 2013;91(5-6):287-96. doi: 10.1159/000350394. Epub 2013 Jun 1.