PMID- 21789884
OWN - NLM
STAT- MEDLINE
DCOM- 20110818
LR  - 20191112
IS  - 0304-4920 (Print)
IS  - 0304-4920 (Linking)
VI  - 53
IP  - 1
DP  - 2010 Feb 28
TI  - Reduction of superior mesenteric hemodynamic responsiveness to [Sar1, 
      Thr8]-angiotensin II and bradykinin, but not sodium nitroprusside, in the 
      presence of homocysteine infusion.
PG  - 45-51
AB  - Hyperhomocysteinemia (HHcy) has been shown to be an independent risk factor for 
      cardiovascular diseases, superior mesenteric thrombosis and inflammatory bowel 
      disease. Superior mesenteric artery (SMA) supplies the intestine and reduced SMA 
      blood flow results in intestinal ischemia. Although in vitro studies have shown 
      that endothelium-dependent vasorelaxation of SMA is reduced in the presence of 
      homocysteine incubation, it is not confirmed with in vivo studies. In this work, 
      we evaluated responsiveness of SMA to endothelium-dependent or -independent 
      vasodilators and a vasoconstrictor in the absence and presence of acute HHcy in 
      vivo to clarify effect of HHcy on superior mesenteric vascular function. Sodium 
      nitroprusside (SNP), bradykinin (BK), and [Sar1,Thr8]angiotensin II 
      ([Sar1,Thr8]-ANG II) were intravenously administrated in sequence in male 
      Sprague-Dawley rats with or without D,L-homocysteine infusion (6 mg/kg/min) 
      through femoral vein. Agonists-induced changes in carotid artery blood pressure, 
      superior mesenteric blood flow and vascular resistance were measured in the 
      present study. We found that acute HHcy infusion had little effects on 
      SNP-induced hemodynamic changes; however, BK-induced changes in blood pressure, 
      blood flow and vascular resistance were significantly reduced in the presence of 
      HHcy infusion. Additionally, HHcy also markedly decreased [Sar1,Thr8]-ANG 
      II-induced superior mesenteric hemodynamic changes. These results demonstrated 
      that responsiveness of SMA to vasoconstrictor, endothelium-dependent, but not 
      endothelium-independent vasodilator, was inhibited in the presence of Hcy 
      infusion. This HHcy-associated vascular hyporesponsiveness to vasoconstrictors 
      and endothelium-dependent vasodilators may partially contribute to circulatory 
      dysfunctions.
FAU - Yen, Chia-Hung
AU  - Yen CH
AD  - Department of Life Science, National Pingtung University of Science and 
      Technology, Pingtung.
FAU - Ma, Yunn-Hwa
AU  - Ma YH
FAU - Yu, Huang-Ping
AU  - Yu HP
FAU - Lau, Ying-Tung
AU  - Lau YT
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - India
TA  - Chin J Physiol
JT  - The Chinese journal of physiology
JID - 7804502
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 11128-99-7 (Angiotensin II)
RN  - 169D1260KM (Nitroprusside)
RN  - S8TIM42R2W (Bradykinin)
SB  - IM
MH  - Angiotensin II/*pharmacology
MH  - Animals
MH  - Blood Pressure/drug effects/physiology
MH  - Bradykinin/*pharmacology
MH  - Endothelium, Vascular/drug effects/physiology
MH  - Hemodynamics/*drug effects/physiology
MH  - Homocysteine/administration & dosage/*pharmacology
MH  - Hyperhomocysteinemia/physiopathology
MH  - Infusions, Intravenous
MH  - Male
MH  - Mesenteric Artery, Superior/drug effects/*physiology
MH  - Models, Animal
MH  - Nitroprusside/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Regional Blood Flow/drug effects/physiology
MH  - Vascular Resistance/drug effects/physiology
EDAT- 2010/02/28 00:00
MHDA- 2011/08/19 06:00
CRDT- 2011/07/28 06:00
PHST- 2011/07/28 06:00 [entrez]
PHST- 2010/02/28 00:00 [pubmed]
PHST- 2011/08/19 06:00 [medline]
AID - 10.4077/cjp.2010.amh065 [doi]
PST - ppublish
SO  - Chin J Physiol. 2010 Feb 28;53(1):45-51. doi: 10.4077/cjp.2010.amh065.